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1.
Cell Mol Biol (Noisy-le-grand) ; 67(6): 74-81, 2022 Feb 27.
Artigo em Inglês | MEDLINE | ID: mdl-35818211

RESUMO

Knee osteoarthritis is the most common joint disease and the most important cause of disability in elderly patients. Due to the side effects of nonsteroidal anti-inflammatory drugs (NSAIDs) in the treatment of osteoarthritis, the use of herbs is recommended as an alternative treatment. The guava fruit can be considered as a natural medicine due to its antioxidant and anti-inflammatory properties. In this study, the effect of Psidium guajava hydroalcoholic extract was considered on reducing the expression of the resistin gene and TNF-α gene in articular chondrocytes of patients with knee osteoarthritis. For this purpose, cartilage chondrocytes of 10 Chinese patients with knee osteoarthritis, who were indicated for arthroplasty, were used for evaluating the effect of guava fruit on the expression of these genes. Articular chondrocytes were cultured under appropriate conditions and their viability was assessed by MTT assay. To increase the level of cytokines, cells were treated with lipopolysaccharide (LPS). They were kept in an incubator with 90% humidity at 37°C for the next steps. Then, the expression of the resistin gene and TNF-α gene was investigated by RNA isolation and cDNA preparation. The results showed that the expression of the resistin gene and TNF-α gene were reduced to 56.59% and 51.86%, respectively, by hydroalcoholic extract of guava fruit. Therefore, according to the results of this study and previous researches, the hydroalcoholic extract of guava fruit (Psidium guajava) can be considered as an effective complementary and alternative treatment for osteoarthritis of the knee.


Assuntos
Osteoartrite do Joelho , Extratos Vegetais , Psidium , Resistina , Fator de Necrose Tumoral alfa , Anti-Inflamatórios/farmacologia , Anti-Inflamatórios/uso terapêutico , Condrócitos , Humanos , Osteoartrite do Joelho/tratamento farmacológico , Osteoartrite do Joelho/genética , Extratos Vegetais/farmacologia , Extratos Vegetais/uso terapêutico , Psidium/química , Resistina/genética , Fator de Necrose Tumoral alfa/genética
2.
J Exp Biol ; 222(Pt 10)2019 05 29.
Artigo em Inglês | MEDLINE | ID: mdl-31085594

RESUMO

The hypothalamus controls metabolism and feeding behaviour via several signals with other tissues. Exercise and supplements can change hypothalamic signalling pathways, so the present study investigated the influence of eccentric resistance training and ß-hydroxy-ß-methylbutyrate free acid supplementation on PGC-1α expression, serum irisin, nesfatin-1 and resistin concentrations. Thirty-two male rats (8 weeks old, 200±17 g body mass) were randomly allocated to control, ß-hydroxy-ß-methylbutyrate free acid supplementation (HMB), eccentric resistance training (ERT), and ß-hydroxy-ß-methylbutyrate free acid supplementation plus eccentric resistance training (HMB+ERT) groups. Training groups undertook eccentric resistance training (6 weeks, 3 times a week) and supplement groups consumed ß-hydroxy-ß-methylbutyrate free acid (HMB-FA) orally (76 mg kg-1 day-1). Twenty-four hours after the last training session, serum and triceps brachii muscle samples were collected and sent to the laboratory for analysis. Two-way ANOVA and Pearson correlation were employed (significance level: P<0.05). The results showed that eccentric resistance training increases skeletal muscle PGC-1α gene expression, as well as serum levels of irisin and nesfatin-1 (P=0.001). Eccentric resistance training decreased the serum concentration of resistin (P=0.001). HMB-FA supplementation increased skeletal muscle PGC-1α gene expression (P=0.002), as well as the serum concentration of irisin and nesfatin-1 (P=0.001), but decreased the serum concentration of resistin (P=0.001). Significant correlations were observed between PGC-1α gene expression and serum concentrations of irisin, nesfatin-1 and resistin. HMB-FA supplementation with eccentric resistance training may induce crosstalk between peptide release from other tissues and increases maximal muscle strength. The combination of the two interventions had a more substantial effect than each in isolation.


Assuntos
Fibronectinas/genética , Nucleobindinas/genética , Coativador 1-alfa do Receptor gama Ativado por Proliferador de Peroxissomo/genética , Ratos/fisiologia , Treinamento Resistido , Resistina/genética , Valeratos/administração & dosagem , Ração Animal/análise , Animais , Dieta , Suplementos Nutricionais/análise , Fibronectinas/sangue , Masculino , Músculo Esquelético/metabolismo , Nucleobindinas/sangue , Coativador 1-alfa do Receptor gama Ativado por Proliferador de Peroxissomo/metabolismo , Distribuição Aleatória , Ratos Sprague-Dawley , Resistina/sangue , Valeratos/metabolismo
3.
Physiol Behav ; 201: 1-11, 2019 03 15.
Artigo em Inglês | MEDLINE | ID: mdl-30552920

RESUMO

Ethanolic extract of leaves of Morus alba L. (M. alba), known as white mulberry, was orally administered (100 mg/kg b.wt) for 8 weeks to female Wistar rats that were fed a high-cholesterol diet (HCD), to investigate the potential of M. alba leaves in attenuation of obesity, dyslipidemia, insulin resistance, and deficits in mood, cognitive as well as motor activity that are linked to the adipokines secretions of visceral adipose tissue. Results showed that M. alba diminished body weight gain, hypercholesterolemia, hypertriglyceridemia, atherogenic (AI) & coronary artery indices (CRI), and ameliorated glucose level and insulin resistance index in rats on HCD, compared with untreated HCD rats. Moreover, M. alba administration significantly decreased serum leptin and resistin contents as well as their mRNA expression in visceral adipose tissue, but significantly increased serum adiponectin level, and its mRNA expression in visceral adipose tissue in rats fed on HCD, compared to those in untreated HCD group. Regarding behavioral alterations, M. alba attenuated motor deficit, declined memory, depression and anxiety-like behavior, as well in rats on HCD, compared to that noticed in untreated HCD rats. The current data showed that serum leptin and resistin showed a positive correlation with and body weight gain, triglycerides (TG), AI as well as CRI, but showed a negative correlation with exploration, declined memory, depression- and anxiety-like behavior. Conversely, serum adiponectin showed a negative correlation with and body weight gain, TG, AI as well as CRI, but showed a positive correlation with locomotor activity, exploration, declined memory, and depression- and anxiety-like behavior. In conclusion, M. alba leaves supplementation could attenuate adiposity, insulin resistance behavioral deficits via down-regulation of regulation of gene expression of leptin, resistin, but up-regulation of adiponectin gene expression in the visceral adipose tissue of rats fed a high-cholesterol diet.


Assuntos
Adiposidade/efeitos dos fármacos , Colesterol na Dieta/farmacologia , Expressão Gênica/efeitos dos fármacos , Resistência à Insulina , Morus/química , Extratos Vegetais/farmacologia , Adiponectina/biossíntese , Adiponectina/genética , Animais , Comportamento Animal/efeitos dos fármacos , Glicemia/metabolismo , Feminino , Hiperlipidemias/tratamento farmacológico , Hiperlipidemias/psicologia , Leptina/biossíntese , Leptina/genética , Folhas de Planta/química , Ratos , Ratos Wistar , Resistina/biossíntese , Resistina/genética , Aumento de Peso/efeitos dos fármacos
4.
Sci Rep ; 8(1): 3921, 2018 03 02.
Artigo em Inglês | MEDLINE | ID: mdl-29500410

RESUMO

S-resistin, a non-secretable resistin isoform, acts as an intracrine factor that regulates adipocyte maduration, inflammatory and insulin response in 3T3-L1 cells. However, its intracellular function in vivo is still unknown. In this study, we analyze the central role of s-resistin, decreasing its hypothalamic expression using an intracerebroventricular injection of lentiviral RNAi. The data present herein support an improvement in the hypothalamic leptin and insulin signaling pathway upon s-resistin downregulation. Furthermore, hypothalamic levels of pro-inflammatory markers decrease, meanwhile those of the anti-inflammatory cytokine IL-10 increases. Interestingly, peripheral NEFA decreases alike circulating leptin and resistin levels. These data demonstrate that hypothalamic s-resistin controls fuel mobilization and adipokines secretion. Importantly, central s-resistin downregulation improves systemic insulin sensitivity, as demonstrated after an IPGTT. Interestingly, our data also indicate that s-resistin downregulation could improve hypothalamic inflammation in aged Wistar rats. Altogether, our findings suggest that hypothalamic s-resistin seems to be a key regulator of the brain-fat axis which links inflammation with metabolic homeostasis.


Assuntos
Adipócitos/metabolismo , Hipotálamo/metabolismo , Inflamação/prevenção & controle , Resistência à Insulina , Insulina/metabolismo , Resistina/antagonistas & inibidores , Adipócitos/imunologia , Adipócitos/patologia , Animais , Citocinas/metabolismo , Células HEK293 , Células HeLa , Homeostase , Humanos , Hipotálamo/imunologia , Hipotálamo/patologia , Inflamação/imunologia , Inflamação/metabolismo , Inflamação/patologia , Masculino , Camundongos , RNA Interferente Pequeno/genética , Ratos , Ratos Wistar , Resistina/genética , Resistina/metabolismo
5.
Br J Nutr ; 118(8): 580-588, 2017 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-29056104

RESUMO

A maternal high-fat, high-sucrose (HFS) diet alters offspring glucose and lipid homoeostasis through unknown mechanisms and may be modulated by folic acid. We investigated the effect of a maternal HFS diet on glucose homoeostasis, expression of genes and proteins associated with insulin signalling and lipid metabolism and the effect of prenatal folic acid supplementation (HFS/F) in male rat offspring. Pregnant Sprague-Dawley rats were randomly fed control (CON), HFS or HFS/F diets. Offspring were weaned on CON; at postnatal day 70, fasting plasma insulin and glucose and liver and skeletal muscle gene and protein expression were measured. Treatment effects were assessed by one-way ANOVA. Maternal HFS diet induced higher fasting glucose in offspring v. HFS/F (P=0·027) and down-regulation (P<0·05) of genes coding for v-Akt murine thymoma viral oncogene homolog 2, resistin and v-Raf-1 murine leukaemia viral oncogene homolog 1 (Raf1) in offspring skeletal muscle and acetyl-CoA carboxylase (Acaca), fatty acid synthase and phosphatidylinositol-4,5-biphosphate 3-kinase, catalytic subunit ß in offspring liver. Skeletal muscle neuropeptide Y and hepatic Kruppel-like factor 10 were up-regulated in HFS v. CON offspring (P<0·05). Compared with CON, Acaca and Raf1 protein expression levels were significantly lower in HFS offspring. Maternal HFS induced higher homoeostasis model of assessment index of insulin resistance v. CON (P=0·030) and HFS/F was associated with higher insulin (P=0·016) and lower glucose (P=0·025). Maternal HFS diet alters offspring insulin sensitivity and de novo hepatic lipogenesis via altered gene and protein expression, which appears to be potentiated by folate supplementation.


Assuntos
Dieta Hiperlipídica , Resistência à Insulina , Insulina/sangue , Metabolismo dos Lipídeos , Fenômenos Fisiológicos da Nutrição Materna , Acetil-CoA Carboxilase/genética , Acetil-CoA Carboxilase/metabolismo , Animais , Animais Recém-Nascidos , Glicemia/metabolismo , Regulação para Baixo , Ácido Graxo Sintases/genética , Ácido Graxo Sintases/metabolismo , Feminino , Ácido Fólico/administração & dosagem , Fígado/metabolismo , Masculino , Fosfotransferases (Aceptor do Grupo Álcool)/genética , Fosfotransferases (Aceptor do Grupo Álcool)/metabolismo , Gravidez , Efeitos Tardios da Exposição Pré-Natal , Proteínas Proto-Oncogênicas c-akt/genética , Proteínas Proto-Oncogênicas c-akt/metabolismo , Proteínas Proto-Oncogênicas c-raf/genética , Proteínas Proto-Oncogênicas c-raf/metabolismo , Ratos , Ratos Sprague-Dawley , Resistina/genética , Resistina/metabolismo , Regulação para Cima
6.
Zhong Nan Da Xue Xue Bao Yi Xue Ban ; 42(7): 790-795, 2017 Jul 28.
Artigo em Chinês | MEDLINE | ID: mdl-28845002

RESUMO

OBJECTIVE: To investigate the effect of acute myocardial infarction (AMI)-activated inflammation on adipokine imbalance and the therapeutic effects of statin.
 Methods: A total of 32 C57BL/6 mice were divided into 4 groups: a sham group, an AMI group, a low-dose atorvastatin [2 mg/(kg.d)] group and a high-dose atorvastatin [20 mg/(kg.d)] group. AMI models were established by surgical coronary artery ligation. Plasma levels of high sensitive C reaction protein (hs-CRP), adiponectin and resistin were measured. Adiponectin and resistin expressions were determined. In addition, mouse 3T3-L1 preadipocytes in vitro were differentiated and they were stimulated by oxidized low density lipoprotein (ox-LDL). The protein expressions of adiponectin and resistin in adipocytes were detected. The effects of atorvastatin on ox-LDL-induced adipokine imbalance in adipocytes were identified.
 Results: The plasma levels of hs-CRP and resistin in AMI mice were significantly increased, whereas the plasma levels of adiponectin were remarkably decreased. However, atorvastatin treatment blocked the changes in the plasma levels of hs-CRP, resistin and adiponectin in AMI mice in a dose-dependent manner. Consistent findings regarding the adipose expressions of the two adipokines were obtained. The plasma levels of hs-CRP were positively correlated with resistin but negatively with adiponectin. In vitro study, ox-LDL increased resistin protein and adiponectin expressions in adipocytes, which were dose-dependently reversed by atorvastatin.
 Conclusion: Inflammation activation in AMI mice leads to adipokine imbalance. Atorvastatin ameliorates the AMI-induced adipokine imbalance via anti-inflammation.


Assuntos
Adipocinas , Atorvastatina/farmacologia , Atorvastatina/uso terapêutico , Infarto do Miocárdio/tratamento farmacológico , Adiponectina/sangue , Adiponectina/genética , Animais , Anti-Inflamatórios/farmacologia , Anti-Inflamatórios/uso terapêutico , Proteína C-Reativa/análise , Expressão Gênica , Inflamação/tratamento farmacológico , Inflamação/fisiopatologia , Camundongos , Camundongos Endogâmicos C57BL , Resistina/sangue , Resistina/genética
7.
PLoS One ; 11(4): e0153198, 2016.
Artigo em Inglês | MEDLINE | ID: mdl-27055280

RESUMO

The neuroendocrine effects of leptin on metabolism hold promise to be translated into a complementary therapy to traditional insulin therapy for diabetes and obesity. However, injections of leptin can provoke inflammation. We tested the effects of leptin, produced in the physiological adipocyte location, on metabolism in mouse models of genetic and dietary obesity. We generated 3T3-L1 adipocytes constitutively secreting leptin and encapsulated them in a poly-L-lysine membrane, which protects the cells from immune rejection. Ob/ob mice (OB) were injected with capsules containing no cells (empty, OB[Emp]), adipocytes (OB[3T3]), or adipocytes overexpressing leptin (OB[Lep]) into both visceral fat depots. Leptin was found in the plasma of OB[Lep], but not OB[Emp] and OB[3T3] mice at the end of treatment (72 days). The OB[Lep] and OB[3T3] mice have transiently suppressed appetite and weight loss compared to OB[Emp]. Only OB[Lep] mice have greater brown fat mass, metabolic rate, and reduced resistin plasma levels compared to OB[Emp]. Glucose tolerance was markedly better in OB[Lep] vs. OB[Emp] and OB[3T3] mice as well as in wild type mice with high-fat diet-induced obesity and insulin resistance treated with encapsulated leptin-producing adipocytes. Our proof-of-principle study provides evidence of long-term improvement of glucose tolerance with encapsulated adipocytes producing leptin.


Assuntos
Adipócitos/metabolismo , Tecido Adiposo Marrom/patologia , Intolerância à Glucose/prevenção & controle , Leptina/metabolismo , Obesidade/fisiopatologia , Resistina/metabolismo , Células 3T3-L1 , Adipócitos/citologia , Tecido Adiposo Marrom/metabolismo , Animais , Western Blotting , Diferenciação Celular , Células Cultivadas , Intolerância à Glucose/genética , Intolerância à Glucose/metabolismo , Resistência à Insulina , Leptina/genética , Masculino , Camundongos , Camundongos Obesos , RNA Mensageiro/genética , Reação em Cadeia da Polimerase em Tempo Real , Resistina/genética , Reação em Cadeia da Polimerase Via Transcriptase Reversa
8.
J Dairy Sci ; 99(2): 1549-1559, 2016 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-26686707

RESUMO

The transition from pregnancy to lactation is characterized by major changes in glucose and adipose tissue metabolism. Anti- and prolipolytic pathways mediated via the hydroxycarboxylic acid receptors 1 (HCAR1) and 2 (HCAR2) and tumor necrosis factor-α receptor 1 (TNFR1), as well as the adipokines apelin and resistin, are likely involved in regulating these processes. This study aimed to determine the mRNA abundance of the aforementioned receptors in both subcutaneous and visceral adipose tissue, to characterize the adipokine concentrations in serum, and to test the effects of feeding diets with either high or low portions of concentrate and a concomitant niacin supplementation from late gestation to early lactation. Twenty pluriparous German Holstein cows were all kept on the same silage-based diet until d 42 antepartum, when they were allocated to 2 feeding groups: until d 1 antepartum, 10 animals each were assigned to either a high-concentrate (60:40 concentrate-to-roughage ratio) or a low-concentrate diet (30:70). Both groups were further subdivided into a control and a niacin group, the latter receiving 24 g/d of nicotinic acid from d -42 until 24. From d 1 to 24 postpartum, the concentrate portion was increased from 30 to 50% for all cows. Biopsies of subcutaneous (SCAT) and retroperitoneal adipose tissue (RPAT) were taken at d -42, 1, 21, and 100 relative to parturition. Blood samples were drawn along with the biopsies and on d -14, 3, 7, 14, and 42. The concentrations of the adipokines apelin and resistin in serum were measured via ELISA. The mRNA of the 3 receptors in AT was quantified as well as the protein abundance of HCAR2 by Western blot. The feeding regimen did not affect the variables examined. The concentrations of apelin remained fairly constant during the observation period, whereas the resistin concentrations increased toward parturition and decreased to precalving levels within 1 wk after calving. The mRNA abundance of HCAR1, HCAR2, and TNFR1 changed in SCAT and RPAT during the considered time period. For the HCAR2 protein, time-dependent changes were restricted to SCAT. The mRNA abundance of all receptors was greater in RPAT than in SCAT. The tissue-specific correlations observed between the receptors point to a link between these factors and may indicate different regulatory roles in the respective tissues. This study provides insight into the complex metabolic adaptations during the transition period and supports a differential regulation of lipolysis among SCAT and RPAT in dairy cows.


Assuntos
Adipocinas/metabolismo , Tecido Adiposo/metabolismo , Bovinos/fisiologia , Gordura Intra-Abdominal/metabolismo , Resistina/metabolismo , Adipocinas/genética , Animais , Dieta/veterinária , Fibras na Dieta/análise , Suplementos Nutricionais/análise , Feminino , Lactação , Lipólise , Parto , Período Pós-Parto , Gravidez , Receptores de Adipocina/genética , Receptores de Adipocina/metabolismo , Resistina/genética , Silagem/análise
9.
Arch Iran Med ; 17(8): 563-8, 2014 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-25065280

RESUMO

BACKGROUND: Recent evidence has indicated that polyunsaturated fatty acids (PUFA), such as omega-3 PUFA, have protective effects on a range of chronic inflammatory conditions, including obesity, and may play a role in the reversal of steatohepatitis. However, the effects of omega-3 PUFA on adipokine expression and hepatic lipid metabolism have not been well evaluated. Thus, the aim of our study was to investigate the effects of PUFAs on adipokines, as well as lipid and glycometabolism, in a rat model of non-alcoholic steatohepatitis (NASH). METHODS: Male Sprague-Dawley rats were divided into control, model and therapy groups. The control group received a normal diet, while the model and therapy groups received a high-fat diet. On the eighth week of high-fat diet, the therapy group was treated with omega-3 PUFA (1.0 g/d) daily. At the end of 20 weeks, serum biochemistry indices were measured and adipokine levels in serum and liver samples were detected with ELISA, Western blotting and real time fluorescence quantitative PCR (qRT-PCR). RESULTS: The weight, biochemical parameters and adipokine levels in serum of the model group were elevated compared to the control group (P < 0.05). In addition, the protein and mRNA expression levels of adipokines in the liver were significantly altered compared to the control group (P < 0.01). The therapy group was characterized by decreased weight and biochemical indices (P < 0.05) compared with the model group. Supplementing high-fat diet with omega-3 PUFA decreased serum levels of leptin and resistin, while adiponectin levels were slightly elevated. In liver tissue samples, the protein and mRNA expression levels of adipokines were significantly improved (P < 0.01) in the therapy group compared to the model group. CONCLUSION: Omega-3 PUFA improved lipid and glycometabolism in NASH rats and regulated adipokine expression, indicating that omega-3 PUFA may have a therapeutic benefit for patients with NASH.


Assuntos
Adipocinas/genética , Ácidos Graxos Ômega-3/farmacologia , Fígado/efeitos dos fármacos , Hepatopatia Gordurosa não Alcoólica/genética , RNA Mensageiro/efeitos dos fármacos , Adipocinas/metabolismo , Adiponectina/genética , Adiponectina/metabolismo , Animais , Dieta Hiperlipídica , Modelos Animais de Doenças , Ácidos Graxos Insaturados , Leptina/genética , Leptina/metabolismo , Fígado/metabolismo , Masculino , Hepatopatia Gordurosa não Alcoólica/metabolismo , RNA Mensageiro/metabolismo , Ratos , Ratos Sprague-Dawley , Resistina/genética , Resistina/metabolismo
10.
Br J Nutr ; 110(10): 1803-9, 2013 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-23632237

RESUMO

Obesity is characterised by chronic low-grade inflammation, and lycopene has been reported to display anti-inflammatory effects. However, it is not clear whether lycopene supplementation modulates adipokine levels in vivo in obesity. To determine whether lycopene supplementation can regulate adipokine expression in obesity, male Wistar rats were randomly assigned to receive a control diet (C, n 6) ora hyperenergetic diet (DIO, n 12) for 6 weeks. After this period, the DIO animals were randomised into two groups: DIO (n 6) and DIO supplemented with lycopene (DIO + L, n 6). The animals received maize oil (C and DIO) or lycopene (DIO + L, 10 mg/kg body weight(BW) per d) by oral administration for a 6-week period. The animals were then killed by decapitation, and blood samples and epididymal adipose tissue were collected for hormonal determination and gene expression evaluation (IL-6, monocyte chemoattractant protein-1(MCP-1), TNF-α, leptin and resistin). There was no detectable lycopene in the plasma of the C and DIO groups. However, the mean lycopene plasma concentration was 24 nmol in the DIO + L group. Although lycopene supplementation did not affect BW or adiposity, it significantly decreased leptin, resistin and IL-6 gene expression in epididymal adipose tissue and plasma concentrations. Also, it significantly reduced the gene expression of MCP-1 in epididymal adipose tissue. Lycopene affects adipokines by reducing leptin, resistin and plasma IL-6 levels. These data suggest that lycopene may be an effective strategy in reducing inflammation in obesity.


Assuntos
Tecido Adiposo/metabolismo , Carotenoides/uso terapêutico , Inflamação/tratamento farmacológico , Interleucina-6/metabolismo , Leptina/metabolismo , Obesidade/tratamento farmacológico , Resistina/metabolismo , Animais , Anti-Inflamatórios/farmacologia , Anti-Inflamatórios/uso terapêutico , Carotenoides/sangue , Carotenoides/farmacologia , Suplementos Nutricionais , Ingestão de Energia , Epididimo , Inflamação/etiologia , Inflamação/genética , Inflamação/metabolismo , Interleucina-6/genética , Leptina/genética , Licopeno , Masculino , Obesidade/complicações , Obesidade/genética , Obesidade/metabolismo , Fitoterapia , Extratos Vegetais/farmacologia , Extratos Vegetais/uso terapêutico , RNA Mensageiro/metabolismo , Distribuição Aleatória , Ratos , Ratos Wistar , Resistina/genética
11.
Regul Pept ; 184: 75-80, 2013 Jun 10.
Artigo em Inglês | MEDLINE | ID: mdl-23518461

RESUMO

Whether leptin targets the hypothalamic serotonergic system to inhibit food intake is not established. We examined the effect of a short-term i.c.v. leptin treatment on serotonin microdialysate levels in rat lateral hypothalamus. Adipose tissue gene expression was also evaluated. Male rats received four daily injections of leptin (5 µg) or vehicle (with pair-feeding to leptin-induced intake) and a fifth injection during collection of LH microdialysates. We found that serotonin and 5-HIAA levels were not affected by the leptin pre-treatment, as basal levels were similar between the leptin and the pair-fed group. These levels remained unaltered after the acute leptin injection. For gene expression studies, rats were pre-treated with five daily injections of either leptin (5 µg) or vehicle (with either pair-feeding or ad libitum intake). mRNA levels of resistin, adiponectin, lipoprotein lipase, and PPAR-gamma were unaltered by either leptin or pair-feeding. Leptin gene expression was significantly reduced by leptin but not by pair-feeding, in both the retroperitoneal (-74%) and the epididymal (-99%) depots while no differences were observed in the subcutaneous depot. The observations confirmed the absence of an acute stimulatory effect of central leptin on serotonin release in the lateral hypothalamus and showed that the pre-treatment with leptin failed to modify this pattern. This indicates that components of the serotonergic system are probably not directly affected by leptin. Additionally, the central effect of leptin was able to downregulate its own adipose tissue gene expression in a depot-specific manner while other adipokine genes were not affected.


Assuntos
Ingestão de Alimentos/efeitos dos fármacos , Hipotálamo/metabolismo , Leptina/farmacologia , Serotonina/metabolismo , Tecido Adiposo/metabolismo , Animais , Ingestão de Alimentos/genética , Expressão Gênica , Ácido Hidroxi-Indolacético/metabolismo , Hipotálamo/efeitos dos fármacos , Leptina/genética , Leptina/metabolismo , Masculino , Microdiálise , RNA Mensageiro/metabolismo , Ratos , Resistina/genética , Resistina/metabolismo
12.
Clin Lab ; 58(1-2): 81-7, 2012.
Artigo em Inglês | MEDLINE | ID: mdl-22372349

RESUMO

BACKGROUND: The goal was to study lipid profiles (TG, TC, LDL, HDL), effects on serum leptin, and fat tissue adiponectin, and resistin as well as body weight effects of Shan He Jian Fei Granules (SHJFG) in rats on a high fat diet. METHODS: Rats were randomly divided into five groups: normal control group fed with normal fat diet, rats on high fat diet receiving low dosage, middle dosage, high dosage of Shan He Jian Fei Granules (SHJFG) as well as a high fat diet group receiving placebo. Rats were treated for 8 weeks. Body weight and naso-anal length of each rat were recorded and Lee's index was calculated. Serum TG, TC, LDL, HDL and leptin concentrations were analyzed. The gene expressions of adiponectin and resistin in adipose tissues were tested by RT-PCR. RESULTS: Compared to the high-fat diet group, body weights, Lee's indexes, weight of fat tissues and serum TG, TC, LDL and leptin of SHJFG groups significantly decreased (p < 0.05), whereas mRNA expressions of adiponectin and resistin of SHJFG groups significantly increased (p < 0.05). CONCLUSIONS: SHJFG could significantly lower body weight and serum TG, TC, and LDL of obese rats. The effects of SHJFG in lowering leptin synthesis and raising mRNA expression of adiponectin and resistin in fat tissues may act as part of the mechanisms in lowering body weight of obese rats. Further studies are needed to demonstrate whether SHJFG may also reduce overall cardiovascular morbidity and mortality like other lipid lowering drugs.


Assuntos
Gorduras na Dieta/administração & dosagem , Medicamentos de Ervas Chinesas/farmacologia , Metabolismo dos Lipídeos/efeitos dos fármacos , Lipídeos/sangue , Obesidade/tratamento farmacológico , Adiponectina/genética , Adiponectina/metabolismo , Tecido Adiposo/efeitos dos fármacos , Tecido Adiposo/metabolismo , Animais , Expressão Gênica/efeitos dos fármacos , Leptina/sangue , Masculino , Obesidade/sangue , RNA Mensageiro/metabolismo , Ratos , Ratos Sprague-Dawley , Resistina/genética , Resistina/metabolismo , Redução de Peso/efeitos dos fármacos
13.
Chem Biol Interact ; 188(3): 457-66, 2010 Dec 05.
Artigo em Inglês | MEDLINE | ID: mdl-20863820

RESUMO

Many benzo[b]furan lignans are known to be biologically active in nature. 2-(3'-Methoxy-4'-hydroxy-phenyl)-5-(3-hydroxypropyl)-7-methoxy-benzo[b]furan-3-carbaldehyde (XH-14) is found as a bioactive component isolated from the plant Salvia miltiorrhiza, commonly known as Danshen, which is a traditional Chinese medicine that is used as a cardiovascular medication. This study examined whether 3 different XH-14 derivatives can inhibit adipocyte differentiation and induction of the adipokines visfatin and resistin in 3T3-L1 adipocytes. Adipocytes were cultured and differentiated in Dulbecco's modified Eagle medium containing fetal bovine serum, 3-isobytyl-1-methylxanthine, dexamethasone, and insulin for 6-8d in the absence and presence of 1-25µM XH-14-derived benzo[b]furan derivatives. Nontoxic 2-(3'-methoxy-4'-hydroxy-phenyl)-6-(3-hydroxypropyl)-5-methoxy-benzo[b]furan (5-MBF) at ≥5µM attenuated cellular lipid accumulation and down-regulated induction of peroxisome proliferator activated receptors γ (PPARγ) and CCAAT enhancer binding protein α (C/EBPα) in a dose-dependent manner, as evidenced by Oil Red O staining and Western blot analysis. Such inhibition of PPAR( and C/EBP( by 5-MBF was achieved at transcriptional mRNA levels. However, 2-(3'-methoxy-4'-hydroxy-phenyl)-5-(3-hydroxypropyl)-7-methoxy-benzo[b]furan (7-MBF) and 2-(3'-methoxy-4'-hydroxy-phenyl)-5-(3-hydroxypropyl)-7-methoxy-benzo[b]furan (6-MBF) had minimal effects on adipogenic differentiation, suggesting a structure-activity relationship of methoxybenzo[b]furan derivatives as an inhibitor of adipogenic differentiation. Furthermore, ≥5µM 5-MBF retarded protein and mRNA expression of proinflammatory and insulin resistance-enhancing adipokines of visfatin and resistin in differentiated adipocytes. Induction of visfatin and resistin was, at least in part, mediated via adipocyte differentiation-associated activation of PPARγ signal targeting adipocyte protein 2 and stearoyl-CoA desaturase. These results demonstrate that the 2-(3'-methoxy-4'-hydroxy-phenyl)-3-hydroxypropyl benzo[b]furan lignan, with a methoxy group at the 5-position on the benzene ring, may be a promising agent for disturbance of adipogenic differentiation and for blockage of obesity-associated inflammatory and metabolic diseases.


Assuntos
Adipogenia/efeitos dos fármacos , Adipocinas/biossíntese , Benzofuranos/química , Benzofuranos/farmacologia , Furanos/química , Furanos/farmacologia , Guaiacol/análogos & derivados , Salvia miltiorrhiza/química , Células 3T3-L1 , Adipócitos/citologia , Adipócitos/efeitos dos fármacos , Adipócitos/metabolismo , Animais , Benzeno/química , Proteína alfa Estimuladora de Ligação a CCAAT/genética , Sobrevivência Celular/efeitos dos fármacos , Indução Enzimática/efeitos dos fármacos , Regulação Enzimológica da Expressão Gênica/efeitos dos fármacos , Guaiacol/química , Guaiacol/farmacologia , Inflamação/genética , Inflamação/metabolismo , Inflamação/patologia , Metabolismo dos Lipídeos/efeitos dos fármacos , Camundongos , Nicotinamida Fosforribosiltransferase/biossíntese , Nicotinamida Fosforribosiltransferase/genética , PPAR gama/genética , Resistina/genética , Relação Estrutura-Atividade
14.
Diab Vasc Dis Res ; 7(3): 231-8, 2010 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-20472602

RESUMO

The RAS is a novel target in the study of diabetes, and clinical trials have indicated that ARBs, such as valsartan, may exert some of their clinical effects through an influence on adipose tissue. We studied the effect of valsartan on adipokine genes resistin (rstn) and fasting-induced adipose factor (fiaf) using obese and diabetic ob/ob mice. In addition to visceral and subcutaneous fat, rstn and fiaf mRNA levels were also measured in several other tissues known to express these adipokines, including the pituitary, cerebral cortex and hypothalamus. The significant findings were that (a) fiaf gene expression was elevated two- to fourfold in visceral and subcutaneous fat from ob/ob mice, compared with lean controls; (b) the increase in fiaf mRNA in subcutaneous, but not visceral, fat from ob/ob mice was returned to lean control levels following 2 weeks of valsartan treatment; (c) fiaf expression was reduced in the hypothalamus, but not in the cortex or pituitary, of ob/ob mice; (d) rstn expression was greatly reduced in visceral fat from ob/ob mice, compared with lean controls, but this was unaffected by valsartan; and (e) rstn expression was unchanged in all other tissues from ob/ob mice, with or without valsartan treatment.


Assuntos
Angiopoietinas/genética , Bloqueadores do Receptor Tipo 1 de Angiotensina II/farmacologia , Diabetes Mellitus/genética , Obesidade/genética , Resistina/genética , Tetrazóis/farmacologia , Valina/análogos & derivados , Proteína 4 Semelhante a Angiopoietina , Animais , Córtex Cerebral/efeitos dos fármacos , Córtex Cerebral/metabolismo , Modelos Animais de Doenças , Regulação da Expressão Gênica/efeitos dos fármacos , Hipotálamo/efeitos dos fármacos , Hipotálamo/metabolismo , Gordura Intra-Abdominal/efeitos dos fármacos , Gordura Intra-Abdominal/metabolismo , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Obesos , Hipófise/efeitos dos fármacos , Hipófise/metabolismo , RNA Mensageiro/metabolismo , Gordura Subcutânea/efeitos dos fármacos , Gordura Subcutânea/metabolismo , Fatores de Tempo , Valina/farmacologia , Valsartana
15.
J Neuroimmunol ; 209(1-2): 96-103, 2009 Apr 30.
Artigo em Inglês | MEDLINE | ID: mdl-19261336

RESUMO

Adipokines that modulate metabolic and inflammatory responses, such as resistin (rstn) and fasting-induced adipose factor (fiaf), are also expressed in mouse brain and pituitary gland. Since lipopolysaccharide (LPS)-induced endotoxinemia provokes an anorectic response via a hypothalamic-dependent mechanism we hypothesized that LPS would also modify hypothalamic adipokine expression. Challenging male CD-1 mice with LPS (5 mg/kg; s.c.) significantly reduced bodyweight (24 h) and realtime RT-PCR revealed time- and tissue-dependent increases in rstn, fiaf and suppressor of cytokine signaling-3 (socs-3) mRNA in hypothalamic, pituitary, cortical and adipose tissues. Gene expression was rapidly increased (3-6 h) in the hypothalamus and pituitary, but returned to normal within 24 h. In contrast, with the exception of rstn in fat, the expression of target genes remained elevated in cortex and visceral fat at 24 h post-injection. In order to more specifically examine the hypothalamic response to LPS we investigated its effects directly on N-1 hypothalamic neurons in vitro. LPS (25 microg/mL; 3 h) had no effect on rstn mRNA, but significantly stimulated fiaf and socs-3 expression. Although various toll-like receptor 4 (TLR4) antagonists (parthenolide, PD098059, and SB202190) did not prevent the LPS-induced increases in fiaf and socs-3, they did partially attenuate its stimulatory effects. We conclude that LPS treatment increases the expression of central, and possibly neuronal, adipokine genes which may influence local tissue repair and function, but could also have downstream consequences on the hypothalamic control of appetite and energy metabolism following an inflammatory insult.


Assuntos
Adipocinas/genética , Encéfalo/metabolismo , Encefalite/metabolismo , Hipófise/metabolismo , Proteínas Supressoras da Sinalização de Citocina/genética , Tecido Adiposo/efeitos dos fármacos , Tecido Adiposo/metabolismo , Tecido Adiposo/fisiopatologia , Proteína 4 Semelhante a Angiopoietina , Angiopoietinas/genética , Animais , Peso Corporal/efeitos dos fármacos , Peso Corporal/fisiologia , Encéfalo/efeitos dos fármacos , Encéfalo/fisiopatologia , Linhagem Celular , Células Cultivadas , Córtex Cerebral/efeitos dos fármacos , Córtex Cerebral/metabolismo , Córtex Cerebral/fisiopatologia , Encefalite/induzido quimicamente , Encefalite/fisiopatologia , Regulação da Expressão Gênica/efeitos dos fármacos , Hipotálamo/efeitos dos fármacos , Hipotálamo/metabolismo , Hipotálamo/fisiopatologia , Mediadores da Inflamação/farmacologia , Lipopolissacarídeos/farmacologia , Masculino , Camundongos , Neurônios/efeitos dos fármacos , Neurônios/metabolismo , Hipófise/efeitos dos fármacos , Hipófise/fisiopatologia , RNA Mensageiro/efeitos dos fármacos , RNA Mensageiro/metabolismo , Resistina/genética , Proteína 3 Supressora da Sinalização de Citocinas , Receptor 4 Toll-Like/antagonistas & inibidores , Receptor 4 Toll-Like/metabolismo
16.
FASEB J ; 23(6): 1946-57, 2009 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-19211925

RESUMO

Omega-3-polyunsaturated fatty acids (omega-3-PUFAs) have well-documented protective effects that are attributed not only to eicosanoid inhibition but also to the formation of novel biologically active lipid mediators (i.e., resolvins and protectins). In this study, we examined their effects on ob/ob mice, an obesity model of insulin resistance and fatty liver disease. Dietary intake of omega-3-PUFAs had insulin-sensitizing actions in adipose tissue and liver and improved insulin tolerance in obese mice. Genes involved in insulin sensitivity (PPARgamma), glucose transport (GLUT-2/GLUT-4), and insulin receptor signaling (IRS-1/IRS-2) were up-regulated by omega-3-PUFAs. Moreover, omega-3-PUFAs increased adiponectin, an anti-inflammatory and insulin-sensitizing adipokine, and induced AMPK phosphorylation, a fuel-sensing enzyme and a gatekeeper of the energy balance. Concomitantly, hepatic steatosis was alleviated by omega-3-PUFAs. A lipidomic analysis with liquid chromatography/mass spectrometry/mass spectrometry revealed that omega-3-PUFAs inhibited the formation of omega-6-PUFA-derived eicosanoids, while triggering the formation of omega-3-PUFA-derived resolvins and protectins. Moreover, representative members of these lipid mediators, namely resolvin E1 and protectin D1, mimicked the insulin-sensitizing and antisteatotic effects of omega-3-PUFAs and induced adiponectin expression to a similar extent that of rosiglitazone, a member of the thiazolidinedione family of antidiabetic drugs. Taken together, these findings uncover beneficial actions of omega-3-PUFAs and their bioactive lipid autacoids in preventing obesity-induced insulin resistance and hepatic steatosis.


Assuntos
Ácidos Docosa-Hexaenoicos/metabolismo , Ácido Eicosapentaenoico/análogos & derivados , Ácidos Graxos Ômega-3 , Fígado Gorduroso/dietoterapia , Fígado Gorduroso/metabolismo , Resistência à Insulina , Obesidade , Proteínas Quinases Ativadas por AMP/metabolismo , Adiponectina/genética , Adiponectina/metabolismo , Tecido Adiposo/citologia , Tecido Adiposo/metabolismo , Animais , Quimiocina CCL2/genética , Quimiocina CCL2/metabolismo , Dieta , Gorduras na Dieta/metabolismo , Ácido Eicosapentaenoico/metabolismo , Ácidos Graxos Ômega-3/química , Ácidos Graxos Ômega-3/metabolismo , Ácidos Graxos Ômega-3/uso terapêutico , Fígado Gorduroso/patologia , Transportador de Glucose Tipo 4/genética , Transportador de Glucose Tipo 4/metabolismo , Hipoglicemiantes/metabolismo , Proteínas Substratos do Receptor de Insulina/genética , Proteínas Substratos do Receptor de Insulina/metabolismo , Masculino , Camundongos , Camundongos Obesos , Músculo Esquelético/metabolismo , Obesidade/metabolismo , Obesidade/patologia , PPAR gama/genética , PPAR gama/metabolismo , Resistina/genética , Resistina/metabolismo , Rosiglitazona , Tiazolidinedionas/metabolismo
17.
Neurosci Lett ; 432(1): 73-8, 2008 Feb 13.
Artigo em Inglês | MEDLINE | ID: mdl-18178314

RESUMO

UNLABELLED: Traumatic brain injury (TBI) induces cachexia and neuroinflammation which profoundly impact patient recovery. Adipokine genes such as leptin (ob), resistin (rstn) and fasting-induced adipose factor (fiaf) are implicated in energy metabolism and body weight control and are also associated with chronic low grade inflammation. Since central rstn and fiaf expression was increased following hypoxic/ischemic brain injury, we hypothesized that these genes would also be induced in the rat brain following TBI. Realtime RT-PCR detected a 2-2.5-fold increase in ob mRNA in the ipsilateral cortex and thalamus 12h following lateral fluid percussion (FP)-induced brain injury. Fiaf mRNA was elevated 5-7.5-fold in cortex, hippocampus and thalamus, and modest increases were also detectable in the contralateral brain. Remarkably, rstn mRNA was elevated in ipsilateral (150-fold) and in contralateral (50-fold) hippocampus. To test whether these changes were part of an inflammatory response to TBI we also examined the effects of an intracerebral injection of lipopolysaccharide (LPS). We determined that central injection of LPS produced some, but not all, of the changes seen after TBI. For example, in contrast to the stimulatory influence of TBI, LPS had no effect on ob expression in any brain region, though fiaf and rstn mRNA levels were significantly elevated in both ipsi- and contralateral cortex. IN CONCLUSION: (a) brain-derived adipokines could be involved in the acute pathology of traumatic brain injury partly through modulation of central inflammatory responses, but also via leptin-mediated neuroprotective effects and (b) TBI-induced brain adipokines may induce the metabolic changes observed following neurotrauma.


Assuntos
Adipocinas/genética , Lesões Encefálicas/fisiopatologia , Encéfalo/fisiologia , Córtex Cerebral/fisiologia , Proteína 4 Semelhante a Angiopoietina , Angiopoietinas , Animais , Lesões Encefálicas/imunologia , Encefalite/fisiopatologia , Metabolismo Energético/fisiologia , Expressão Gênica/fisiologia , Hipotálamo/fisiologia , Leptina/genética , Lipopolissacarídeos/farmacologia , Masculino , RNA Mensageiro/metabolismo , Ratos , Ratos Sprague-Dawley , Resistina/genética , Tálamo/fisiologia
18.
Neuroendocrinology ; 85(4): 232-41, 2007.
Artigo em Inglês | MEDLINE | ID: mdl-17579277

RESUMO

Adipokines such as leptin, resistin, and fasting-induced adipose factor (FIAF) are secreted by adipocytes, but their expression is also detectable in the brain and pituitary. The role of central adipokines remains elusive, but we speculate that they may modulate those hypothalamic signaling pathways that control energy homeostasis. Here we describe experiments to test this in which we exploited a novel hypothalamic neuronal cell line (N-1) that expresses a variety of neuropeptides and receptors that are known to be implicated in appetite regulation. Using real-time RT-PCR, we confirmed that N-1 neurons express resistin (rstn) and fiaf, as well as suppressor of cytokine signaling-3 (socs-3), a feedback inhibitor of leptin signaling. Treating N-1 cells with recombinant resistin (200 ng/ml, 30 min) reduced both fiaf (25%, p < 0.005) and socs-3 (29%, p < 0.005) mRNA levels, and similar reductions in fiaf (40%, p < 0.001) and socs-3 (25%, p < 0.001) resulted following the overexpression of resistin. Conversely, when RNA interference (RNAi) was used to reduce endogenous rstn levels (-60%, p < 0.005), fiaf and socs-3 expression was increased (46 and 65% respectively, p < 0.005). A similar reduction in rstn mRNA was achieved using RNAi in differentiated 3T3-L1 adipocytes, and this manipulation also reduced fiaf and socs-3 expression (-53, -21 and -20% respectively, p < 0.005). In contrast, although RNAi successfully reduced fiaf mRNA by 50% (p < 0.001) in N-1 cells and 40% (p < 0.001) in 3T3-L1 cells, there was no effect on rstn or socs-3 mRNA. These data suggest that resistin exerts a novel autocrine/paracrine control over fiaf and socs-3 expression in both 3T3-L1 adipocytes and N-1 neurons. Such a mechanism could be part of the central feedback system that modulates the effects of adipokines, and other adiposity signals, implicated in hypothalamic energy homeostasis. However, it remains to be determined whether these in vitro results can be translated to the control of adipokine expression in brain and adipose tissue.


Assuntos
Proteínas Sanguíneas/genética , Hipotálamo/metabolismo , Neurônios/metabolismo , Resistina/farmacologia , Proteínas Supressoras da Sinalização de Citocina/genética , Células 3T3-L1 , Adiponectina/genética , Adiponectina/metabolismo , Proteína 4 Semelhante a Angiopoietina , Angiopoietinas , Animais , Comunicação Autócrina/genética , Proteínas Sanguíneas/metabolismo , Linhagem Celular , Regulação da Expressão Gênica/efeitos dos fármacos , Hipotálamo/citologia , Camundongos , Comunicação Parácrina/genética , Interferência de RNA , Resistina/genética , Resistina/metabolismo , Proteína 3 Supressora da Sinalização de Citocinas , Proteínas Supressoras da Sinalização de Citocina/metabolismo , Transfecção
19.
J Clin Invest ; 117(6): 1670-8, 2007 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-17525801

RESUMO

Circulating resistin stimulates endogenous glucose production (GP). Here, we report that bi-directional changes in hypothalamic resistin action have dramatic effects on GP and proinflammatory cytokine expression in the liver. The infusion of either resistin or an active cysteine mutant in the third cerebral ventricle (icv) or in the mediobasal hypothalamus stimulated GP independent of changes in circulating levels of glucoregulatory hormones. Conversely, central antagonism of resistin action markedly diminished the ability of circulating resistin to enhance GP. We also report that centrally mediated mechanisms partially control resistin-induced expression of TNF-alpha, IL-6, and SOCS-3 in the liver. These results unveil what we believe to be a novel site of action of resistin on GP and inflammation and suggest that hypothalamic resistin action can contribute to hyperglycemia in type 2 diabetes mellitus.


Assuntos
Hipotálamo/metabolismo , Resistência à Insulina/fisiologia , Fígado/metabolismo , Resistina/metabolismo , Animais , Citocinas/genética , Diabetes Mellitus Tipo 2/etiologia , Diabetes Mellitus Tipo 2/genética , Diabetes Mellitus Tipo 2/metabolismo , Gluconeogênese/efeitos dos fármacos , Humanos , Mediadores da Inflamação/metabolismo , Injeções Intraventriculares , Fígado/efeitos dos fármacos , Masculino , Mutagênese Sítio-Dirigida , Obesidade/complicações , Obesidade/genética , Obesidade/metabolismo , Ratos , Ratos Sprague-Dawley , Proteínas Recombinantes/genética , Proteínas Recombinantes/metabolismo , Proteínas Recombinantes/farmacologia , Resistina/genética , Resistina/farmacologia
20.
Br J Nutr ; 97(6): 1074-82, 2007 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-17381975

RESUMO

It is known that conjugated linoleic acid (CLA) feeding decreases body adiposity but the mechanisms involved are not clear. The aim of this study was to analyse whether alterations in uncoupling protein (UCP) expression in white and brown adipose tissues (WAT and BAT, respectively) and in skeletal muscle may be responsible for the effect of trans-10, cis-12 CLA on the size of body fat depots in hamsters. Animals were divided into three groups and fed an atherogenic diet with different amounts of trans-10, cis-12 CLA (0 control, 0.5, or 1 g/100 g diet) for 6 weeks. CLA feeding reduced adipose depot weights, but had no effect on body weight. Leptin mRNA expression decreased in both subcutaneous and perirenal WAT depots, in accordance with lower adiposity, whereas resistin mRNA expression was not changed. Animals fed CLA had lower UCP1 mRNA levels in BAT (both doses of CLA) and in perirenal WAT (the low dose), and lower UCP3 mRNA levels in subcutaneous WAT (the high dose). UCP2 mRNA expression in WAT was not significantly affected by CLA feeding. Animals fed the high dose of CLA showed increased UCP3 and carnitine palmitoyl transferase-I (CPT-I) mRNA expression levels in skeletal muscle. In summary, induction of UCP1 or UCP2 in WAT and BAT is not likely to be responsible for the fat-reduction action of CLA, but the increased expression of UCP3 in skeletal muscle, together with a higher expression of CPT-I, may explain the previously reported effects of dietary CLA in lowering adiposity and increasing fatty acid oxidation by skeletal muscle.


Assuntos
Dieta Aterogênica , Canais Iônicos/biossíntese , Ácidos Linoleicos Conjugados/farmacologia , Proteínas Mitocondriais/biossíntese , Tecido Adiposo/anatomia & histologia , Tecido Adiposo/efeitos dos fármacos , Tecido Adiposo/metabolismo , Animais , Northern Blotting/métodos , Peso Corporal/efeitos dos fármacos , Cricetinae , Suplementos Nutricionais , Relação Dose-Resposta a Droga , Ingestão de Alimentos/efeitos dos fármacos , Regulação da Expressão Gênica/efeitos dos fármacos , Canais Iônicos/genética , Leptina/biossíntese , Leptina/genética , Masculino , Mesocricetus , Proteínas Mitocondriais/genética , Músculo Esquelético/anatomia & histologia , Músculo Esquelético/efeitos dos fármacos , Músculo Esquelético/metabolismo , RNA Mensageiro/genética , Resistina/biossíntese , Resistina/genética , Reação em Cadeia da Polimerase Via Transcriptase Reversa/métodos , Proteína Desacopladora 1
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