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1.
Medicina (Kaunas) ; 56(5)2020 May 06.
Artículo en Inglés | MEDLINE | ID: mdl-32384612

RESUMEN

Background and objectives: The practice of physical exercise, especially resistance exercise, is important for the treatment and/or prevention of cardiovascular risk factors in adult individuals. However, there are few studies on its effects on adolescent individuals. Therefore, the aim of the present study was to evaluate the effects of applying a 12-week resistance training program on cardiovascular risk factors in adolescents. Materials and Methods: Thus, 122 adolescents aged 13-16 years of both genders participated in the study from school in the city of Lagarto, Sergipe (SE), Brazil, divided into two groups: Control Group (CG) and Group undergoing resistance training (RTG). Blood collection and anthropometric measurements were performed before and after the 12-week resistance training program (RTP). Results: After 12 weeks of the RTP in the adolescents, there was a reduction in the triglyceride variables (9.55%, p = 0.0286), Low-Density Lipoproteins (LDL) (5.42%, p = 0.0244), non-High-Density Lipoproteins (HDL) (5.40%, p = 0.0019), blood glucose (6.71%, p = 0.0040), systolic blood pressure (10.13%, p < 0.0001), as well as an increase in the body weight variable (1.73%, p = 0.0003). Conclusions: It was concluded that a 12-week RTP can prevent and/or alleviate the development of several chronic degenerative diseases in adulthood and that resistance training is important for maintaining the health of adolescents.


Asunto(s)
Factores de Riesgo de Enfermedad Cardiaca , Entrenamiento de Fuerza/normas , Adolescente , Brasil , Femenino , Humanos , Masculino , Obesidad/fisiopatología , Obesidad/terapia , Entrenamiento de Fuerza/métodos , Factores de Riesgo , Instituciones Académicas/organización & administración , Instituciones Académicas/estadística & datos numéricos
2.
FASEB J ; 31(5): 1976-1986, 2017 05.
Artículo en Inglés | MEDLINE | ID: mdl-28138038

RESUMEN

Cancer cachexia is a multifactorial syndrome characterized by body weight loss, atrophy of adipose tissue (AT) and systemic inflammation. However, there is limited information regarding the mechanisms of immunometabolic response in AT from cancer cachexia. Male Wistar rats were inoculated with 2 × 107 of Walker 256 tumor cells [tumor bearing (TB) rats]. The mesenteric AT (MeAT) was collected on d 0, 4, 7 (early stage), and 14 (cachexia stage) after tumor cell injection. Surgical biopsies for MeAT were obtained from patients who had gastrointestinal cancer with cachexia. Lipolysis showed an early decrease in glycerol release in TB d 4 (TB4) rats in relation to the control, followed by a 6-fold increase in TB14 rats, whereas de novo lipogenesis was markedly lower in the incorporation of glucose into fatty acids in TB14 rats during the development of cachexia. CD11b and CD68 were positive in TB7 and TB14 rats, respectively. In addition, we found cachexia stage results similar to those of animals in MeAT from patients: an increased presence of CD68+, iNOS2+, TNFα+, and HSL+ cells. In summary, translational analysis of MeAT from patients and an animal model of cancer cachexia enabled us to identify early disruption in Adl turnover and subsequent inflammatory response during the development of cancer cachexia.-Henriques, F. S., Sertié, R. A. L., Franco, F. O., Knobl, P., Neves, R. X., Andreotti, S., Lima, F. B., Guilherme, A., Seelaender, M., Batista, M. L., Jr. Early suppression of adipocyte lipid turnover induces immunometabolic modulation in cancer cachexia syndrome.


Asunto(s)
Adipocitos/metabolismo , Tejido Adiposo/metabolismo , Caquexia/etiología , Caquexia/metabolismo , Metabolismo de los Lípidos , Neoplasias/complicaciones , Neoplasias/metabolismo , Animales , Ácidos Grasos/metabolismo , Inflamación/metabolismo , Metabolismo de los Lípidos/fisiología , Masculino , Ratas Wistar
3.
Physiol Genomics ; 49(12): 712-721, 2017 Dec 01.
Artículo en Inglés | MEDLINE | ID: mdl-28986396

RESUMEN

Emerging evidence suggests that both systemic and white adipose tissue-renin-angiotensin system components influence body weight control. We previously demonstrated that higher angiotensin-converting enzyme (ACE) gene expression is associated with lower body adiposity in a rodent model. In this study, we tested the hypothesis that a higher ACE gene dosage reduces fat accumulation by increasing energy expenditure and modulating lipolysis and glucose incorporation into lipids in adipocytes. After a 12 wk follow-up period, transgenic mice harboring three ACE (3ACE) gene copies displayed diminished WAT mass, lipid content in their carcasses, adipocyte hypotrophy, and higher resting oxygen uptake (V̇o2) in comparison with animals with one ACE gene copy (1ACE) after long fasting (12 h). No differences were found in food intake and in the rates of lipolysis and glucose incorporation into lipids in adipocytes. To assess whether this response involves increased angiotensin II type I receptor (AT1R) activation, AT1R blocker (losartan) was used in a separate group of 3ACE mice with body weight and adiposity comparable to that in the other 3ACE animals. We suggest that fasting-induced lower adiposity observed in animals with 3ACE gene copies might be associated with a higher expense of energy reserves; this response did not involve AT1R activation.


Asunto(s)
Glucosa/metabolismo , Tejido Adiposo/metabolismo , Adiposidad/genética , Adiposidad/fisiología , Metabolismo Energético/genética , Metabolismo Energético/fisiología , Lipólisis
4.
J Pineal Res ; 58(3): 251-61, 2015 Apr.
Artículo en Inglés | MEDLINE | ID: mdl-25626464

RESUMEN

Melatonin, the main hormone produced by the pineal gland, is secreted in a circadian manner (24-hr period), and its oscillation influences several circadian biological rhythms, such as the regulation of clock genes expression (chronobiotic effect) and the modulation of several endocrine functions in peripheral tissues. Assuming that the circadian synchronization of clock genes can play a role in the regulation of energy metabolism and it is influenced by melatonin, our study was designed to assess possible alterations as a consequence of melatonin absence on the circadian expression of clock genes in the epididymal adipose tissue of male Wistar rats and the possible metabolic repercussions to this tissue. Our data show that pinealectomy indeed has impacts on molecular events: it abolishes the daily pattern of the expression of Clock, Per2, and Cry1 clock genes and Pparγ expression, significantly increases the amplitude of daily expression of Rev-erbα, and affects the pattern of and impairs adipokine production, leading to a decrease in leptin levels. However, regarding some metabolic aspects of adipocyte functions, such as its ability to synthesize triacylglycerols from glucose along 24 hr, was not compromised by pinealectomy, although the daily profile of the lipogenic enzymes expression (ATP-citrate lyase, malic enzyme, fatty acid synthase, and glucose-6-phosphate dehydrogenase) was abolished in pinealectomized animals.


Asunto(s)
Tejido Adiposo Blanco/metabolismo , Ritmo Circadiano/genética , Expresión Génica/genética , Proteínas Circadianas Period/metabolismo , Glándula Pineal , Animales , Ritmo Circadiano/fisiología , Expresión Génica/fisiología , Masculino , Proteínas Circadianas Period/genética , Glándula Pineal/enzimología , Glándula Pineal/fisiología , Glándula Pineal/cirugía , Ratas , Ratas Wistar
5.
Mol Cell Endocrinol ; 589: 112250, 2024 Aug 01.
Artículo en Inglés | MEDLINE | ID: mdl-38663485

RESUMEN

The most common form of hypercortisolism is iatrogenic Cushing's syndrome. Lipodystrophy and metabolic disorders can result from the use of exogenous glucocorticoids (GC). Adipocytes play an important role in the production of circulating exosomal microRNAs, and knockdown of Dicer promotes lipodystrophy. The aim of this study is to investigate the effect of GCs on epididymal fat and to assess their influence on circulating microRNAs associated with fat turnover. The data indicate that despite the reduction in adipocyte volume due to increased lipolysis and apoptosis, there is no difference in tissue mass, suggesting that epididymal fat pad, related to animal size, is not affected by GC treatment. Although high concentrations of GC have no direct effect on epididymal microRNA-150-5p expression, GC can induce epididymal adipocyte uptake of microRNA-150-5p, which regulates transcription factor Ppar gamma during adipocyte maturation. In addition, GC treatment increased lipolysis and decreased glucose-derived lipid and glycerol incorporation. In conclusion, the similar control and GC epididymal fat mass results from increased dense fibrogenic tissue and decreased adipocyte volume induced by the lipolytic effect of GC. These findings demonstrate the complexity of epididymal fat. They also highlight how this disease alters fat distribution. This study is the first in a series published by our laboratory showing the detailed mechanism of adipocyte turnover in this disease.


Asunto(s)
Adipocitos , Epidídimo , Glucocorticoides , Lipólisis , MicroARNs , Masculino , Animales , MicroARNs/metabolismo , MicroARNs/genética , Epidídimo/efectos de los fármacos , Epidídimo/metabolismo , Epidídimo/patología , Adipocitos/efectos de los fármacos , Adipocitos/metabolismo , Glucocorticoides/efectos adversos , Glucocorticoides/farmacología , Lipólisis/efectos de los fármacos , Ratones , Apoptosis/efectos de los fármacos , Ratones Endogámicos C57BL , PPAR gamma/metabolismo , PPAR gamma/genética
6.
Front Endocrinol (Lausanne) ; 14: 1259854, 2023.
Artículo en Inglés | MEDLINE | ID: mdl-38027196

RESUMEN

Background: Intrauterine food restriction (IFR) during pregnancy is associated with low birth weight (LBW) and obesity in adulthood. It is known that white adipose tissue (WAT) plays critical metabolic and endocrine functions; however, this tissue's behavior before weight gain and obesity into adulthood is poorly studied. Thus, we evaluated the repercussions of IFR on the lipogenesis and lipolysis processes in the offspring and described the effects on WAT inflammatory cytokine production and secretion. Methods: We induced IFR by providing gestating rats with 50% of the necessary chow daily amount during all gestational periods. After birth, we monitored the offspring for 12 weeks. The capacity of isolated fat cells from mesenteric white adipose tissue (meWAT) to perform lipogenesis (14C-labeled glucose incorporation into lipids) and lipolysis (with or without isoproterenol) was assessed. The expression levels of genes linked to these processes were measured by real-time PCR. In parallel, Multiplex assays were conducted to analyze pro-inflammatory markers, such as IL-1, IL-6, and TNF-α, in the meWAT. Results: Twelve-week-old LBW rats presented elevated serum triacylglycerol (TAG) content and attenuated lipogenesis and lipolysis compared to control animals. Inflammatory cytokine levels were increased in the meWAT of LBW rats, evidenced by augmented secretion by adipocytes and upregulated gene and protein expression by the tissue. However, there were no significant alterations in the serum cytokines content from the LBW group. Additionally, liver weight, TAG content in the hepatocytes and serum glucocorticoid levels were increased in the LBW group. Conclusion: The results demonstrate that IFR throughout pregnancy yields LBW offspring characterized by inhibited lipogenesis and lipolysis and reduced meWAT lipid storage at 12 weeks. The increased serum TAG content may contribute to the augmented synthesis and secretion of pro-inflammatory markers detected in the LBW group.


Asunto(s)
Adipocitos , Lipogénesis , Embarazo , Femenino , Ratas , Animales , Adipocitos/metabolismo , Lipólisis , Obesidad/metabolismo , Citocinas/metabolismo , Triglicéridos/metabolismo
7.
Front Physiol ; 14: 1161582, 2023.
Artículo en Inglés | MEDLINE | ID: mdl-37234421

RESUMEN

Introduction: Lactation overnutrition is a programming agent of energy metabolism, and litter size reduction leads to the early development of obesity, which persists until adulthood. Liver metabolism is disrupted by obesity, and increased levels of circulating glucocorticoids are pointed as a possible mediator for the obesity development, since bilateral adrenalectomy (ADX) can reduce obesity in different models of obesity. Methods: This study aimed to evaluate the effects of glucocorticoids on metabolic changes and liver lipogenesis and insulin pathway induced by lactation overnutrition. For this, on the postnatal day 3 (PND), 3 pups (small litter-SL) or 10 pups (normal litter-NL) were kept with each dam. On PND 60, male Wistar rats underwent bilateral adrenalectomy (ADX) or fictitious surgery (sham), and half of ADX animals received corticosterone (CORT- 25 mg/L) diluted in the drinking fluid. On PND 74, the animals were euthanized by decapitation for trunk blood collection, and liver dissection and storage. Results and Discussion: SL rats presented increased corticosterone, free fatty acids, total and LDL-cholesterol plasma levels, without changes in triglycerides (TG) and HDL-cholesterol. The SL group also showed increased content of liver TG, and expression of fatty acid synthase (FASN), but decreased expression of PI3Kp110 in the liver, compared to NL rats. In the SL group, the ADX decreased plasma levels of corticosterone, FFA, TG and HDL cholesterol, liver TG, and liver expression of FASN, and IRS2, compared to sham animals. In SL animals, CORT treatment increased plasma levels of TG and HDL cholesterol, liver TG, and expression of FASN, IRS1, and IRS2, compared with the ADX group. In summary, the ADX attenuated plasma and liver changes observed after lactation overnutrition, and CORT treatment could reverse most ADX-induced effects. Thus, increased circulating glucocorticoids are likely to play a pivotal role in liver and plasma impairments induced by lactation overnutrition in male rats.

8.
J Biol Rhythms ; 35(6): 530-541, 2020 12.
Artículo en Inglés | MEDLINE | ID: mdl-32886018

RESUMEN

In adipose tissue, the expression of hundreds of genes exhibits circadian oscillation, which may or may not be affected by circulating melatonin levels. Using control and pinealectomized rats, we investigated the daily expression profile of Actb, Hprt-1, B2m, and Rpl37a, genes that are commonly used as reference genes for reverse transcription quantitative polymerase chain reaction (RT-qPCR), in epididymal (EP), retroperitoneal (RP), and subcutaneous (SC) adipose tissues. In control rats, Actb expression presented a daily oscillation in all adipose tissues investigated, Hprt-1 showed 24-h fluctuations in only RP and SC depots, B2m was stable over 24 h for EP and RP but oscillated over 24 h in SC adipose tissue, and Rpl37a presented a daily oscillation in only RP fat. In the absence of melatonin, the rhythmicity of Actb in all adipose depots was abolished, the daily rhythmicity of Hprt-1 and B2m was disrupted in SC fat, the peak expression of Rpl37a and Hprt-1 was delayed, and the amplitude of Rpl37a was reduced in RP adipose tissue. Collectively, our results demonstrate that the expression of putative reference genes displays a daily rhythm influenced by melatonin levels in a manner specific to the adipose depot. Thus, the proper standardization and daily profile expression of reference genes should be performed carefully in temporal studies using RT-qPCR analysis.


Asunto(s)
Tejido Adiposo Blanco/metabolismo , Ritmo Circadiano/genética , Regulación de la Expresión Génica , Melatonina/metabolismo , Animales , Masculino , Pinealectomía , Ratas , Ratas Wistar , Reacción en Cadena en Tiempo Real de la Polimerasa , Valores de Referencia
9.
Nutrients ; 13(1)2020 Dec 31.
Artículo en Inglés | MEDLINE | ID: mdl-33396291

RESUMEN

Diabetes mellitus is one of the most prevalent chronic diseases in the world; one of its main characteristics is chronic hyperglycemia. Pharmacotherapy and other alternatives such as regular exercise are among the therapeutic methods used to control this pathology and participate in glycemic control, as well as the ingestion of plant extracts with antioxidant effects. Among the different plants used for this purpose, curcumin has potential to be used to attenuate the hyperglycemic condition triggered by diabetes mellitus (DM). Some prior studies suggest that this plant has antioxidant and hypoglycemic potential. This review aims to evaluate the antioxidant and hypoglycemic potential of curcumin supplementation in Type 1 DM (T1DM) and Type 2 DM (T2DM). The search considered articles published between 2010 and 2019 in English and Portuguese, and a theoretical survey of relevant information was conducted in the main databases of scientific publications, including the Virtual Health Library and its indexed databases, PubMed, LILACS (Latin American and Caribbean Literature on Health Sciences-Health Information for Latin America and the Caribbean-BIREME/PAHO/WHO), and Scientific Electronic Library Online (SciELO). The associated use of turmeric and physical exercise has demonstrated antioxidant, anti-inflammatory, and hypoglycemic effects, suggesting that these could be used as potential therapeutic methods to improve the quality of life and survival of diabetic patients.


Asunto(s)
Diabetes Mellitus Tipo 1/terapia , Diabetes Mellitus Tipo 2/terapia , Terapia por Ejercicio , Extractos Vegetales/administración & dosificación , Calidad de Vida , Animales , Antioxidantes/administración & dosificación , Glucemia/análisis , Terapia Combinada/métodos , Curcuma , Diabetes Mellitus Tipo 1/sangre , Diabetes Mellitus Tipo 1/complicaciones , Diabetes Mellitus Tipo 2/sangre , Diabetes Mellitus Tipo 2/complicaciones , Suplementos Dietéticos , Modelos Animales de Enfermedad , Humanos , Hipoglucemiantes/administración & dosificación , Resultado del Tratamiento
10.
Artículo en Inglés | MEDLINE | ID: mdl-32774865

RESUMEN

BACKGROUND: Type 1 diabetes mellitus (T1DM) is a metabolic disease characterized by hyperglycemia and excessive generation of reactive oxygen species caused by autoimmune destruction of beta-cells in the pancreas. Among the antioxidant compounds, Curcuma longa (CL) has potential antioxidant effects and may improve hyperglycemia in uncontrolled T1DM/TD1, as well as prevent its complications (higher costs for the maintenance of health per patient, functional disability, cardiovascular disease, and metabolic damage). In addition to the use of compounds to attenuate the effects triggered by diabetes, physical exercise is also essential for glycemic control and the maintenance of skeletal muscles. Our objective is to evaluate the effects of CL supplementation associated with moderate- to high-intensity resistance training on the parameters of body weight recovery, glycemic control, reactive species markers, and tissue damage in rats with T1DM/TD1. METHODS: Forty male 3-month-old Wistar rats (200-250 g) with alloxan-induced T1DM were divided into 4 groups (n = 7-10): sedentary diabetics (DC); diabetic rats that underwent a 4-week resistance training protocol (TD); CL-supplemented diabetic rats (200 mg/kg body weight, 3x a week) (SD); and supplemented diabetic rats under the same conditions as above and submitted to training (TSD). Body weight, blood glucose, and the following biochemical markers were analyzed: lipid profile, aspartate aminotransferase (AST), alanine aminotransferase (ALT), uric acid, creatine kinase (CK), lactate dehydrogenase (LDH), and thiobarbituric acid reactive substances (TBARS). RESULTS: Compared to the DC group, the TD group showed body weight gain (↑7.99%, p = 0.0153) and attenuated glycemia (↓23.14%, p = 0.0008) and total cholesterol (↓31.72%, p ≤ 0.0041) associated with diminished reactive species markers in pancreatic (↓45.53%, p < 0.0001) and cardiac tissues (↓51.85%, p < 0.0001). In addition, compared to DC, TSD promoted body weight recovery (↑15.44%, p ≤ 0.0001); attenuated glycemia (↓42.40%, p ≤ 0.0001), triglycerides (↓39.96%, p ≤ 0.001), and total cholesterol (↓28.61%, p ≤ 0.05); and attenuated the reactive species markers in the serum (↓26.92%, p ≤ 0.01), pancreas (↓46.22%, p ≤ 0.0001), cardiac (↓55.33%, p ≤ 0.001), and skeletal muscle (↓42.27%, p ≤ 0.001) tissues caused by T1DM. CONCLUSION: Resistance training associated (and/or not) with the use of Curcuma longa attenuated weight loss, the hypoglycemic and hypolipidemic effects, reactive species markers, and T1DM-induced tissue injury.

11.
J Pineal Res ; 47(3): 221-7, 2009 Oct.
Artículo en Inglés | MEDLINE | ID: mdl-19663997

RESUMEN

Considering that melatonin has been implicated in body weight control, this work investigated whether this effect involves the regulation of adipogenesis. 3T3-L1 preadipocytes were induced to differentiate in the absence or presence of melatonin (10(-3) m). Swiss-3T3 cells ectopically and conditionally (Tet-off system) over-expressing the 34 kDa C/EBPbeta isoform (Swiss-LAP cells) were employed as a tool to assess the mechanisms of action at the molecular level. Protein markers of the adipogenic phenotype were analyzed by Western blot. At 36 hr of differentiation of 3T3-L1 preadipocytes, a reduction of PPARgamma expression was detected followed by a further reduction, at day 4, of perilipin, aP2 and adiponectin protein expression in melatonin-treated cells. Real-time PCR analysis also showed a decrease of PPARgamma (60%), C/EBPalpha (75%), adiponectin (30%) and aP2 (40%) mRNA expression. Finally, we transfected Swiss LAP cells with a C/EBPalpha gene promoter/reporter construct in which luciferase expression is enhanced in response to C/EBPbeta activity. Culture of such transfected cells in the absence of tetracycline led to a 2.5-fold activation of the C/EBPalpha promoter. However, when treated with melatonin, the level of C/EBPalpha promoter activation by C/EBPbeta was reduced by 50% (P = 0.05, n = 6). In addition, this inhibitory effect of melatonin was also reflected in the phenotype of the cells, since their capacity to accumulate lipids droplets was reduced as confirmed by the poor staining with Oil Red O. In conclusion, melatonin at a concentration of 10(-3 ) m works as a negative regulator of adipogenesis acting in part by inhibiting the activity of a critical adipogenic transcription factor, C/EBPbeta.


Asunto(s)
Adipocitos/citología , Adipocitos/efectos de los fármacos , Proteína beta Potenciadora de Unión a CCAAT/genética , Diferenciación Celular/efectos de los fármacos , Depresores del Sistema Nervioso Central/farmacología , Regulación de la Expresión Génica/efectos de los fármacos , Melatonina/farmacología , Células 3T3 , Adipocitos/metabolismo , Adiponectina/genética , Animales , Western Blotting , Proteína alfa Potenciadora de Unión a CCAAT/genética , Proteína beta Potenciadora de Unión a CCAAT/metabolismo , Diferenciación Celular/genética , Proteínas de Unión a Ácidos Grasos/genética , Ratones , PPAR gamma/genética , Reacción en Cadena de la Polimerasa , Activación Transcripcional/efectos de los fármacos
12.
Life Sci ; 232: 116683, 2019 Sep 01.
Artículo en Inglés | MEDLINE | ID: mdl-31344430

RESUMEN

AIMS: Previous work has demonstrated that ketogenic diets promote white fat browning; however, the exact mechanisms underlying this phenomenom have yet to be elucidated. Recently, an in vitro study showed that supraphysiological concentrations of ß-hydroxybutyrate (ßHB) had a strong influence on the induction of adipocyte browning. On the other hand, concentrations in the physiological range, achieved through ketogenic diets and prolonged fasting produce values of 1-3 mM and 4-7 mM, respectively. Herein, we investigated the impact of physiological concentrations of ßHB on metabolism, and the expression of uncoupling protein 1 (UCP1) and other browning markers in adipose tissues. MAIN METHODS: The effects of ßHB on adipocyte browning were investigated in vitro, using primary cultures of isolated visceral and subcutaneous fat cells and cultured 3T3-L1 adipocytes, and in vivo. KEY FINDINGS: It was determined that ßHB failed to induce changes in the oxidative capacity, citrate synthase activity or browning gene expression patterns in isolated adipocytes, and did not exert a permissive effect on ß-adrenergic agonist-induced browning. In addition, 3T3-L1 adipocytes differentiated following ßHB treatment exhibited downregulated Ucp1 expression levels, a result that was recapitulated in the subcutaneous adipose tissue of Wistar rats after ßHB salt treatment. Rats administered ßHB salts also presented reduced brown adipose tissue UCP1 protein expression. SIGNIFICANCE: The mechanisms underlying ketogenic diet-induced browning of adipocytes are not known. The results from the present study indicate that physiological concentrations of ßHB are not responsible for this phenomenon, despite the observed ßHB-mediated downregulation of UCP1 expression.


Asunto(s)
Ácido 3-Hidroxibutírico/metabolismo , Tejido Adiposo Pardo/metabolismo , Células 3T3-L1 , Animales , Masculino , Ratones , Ratas , Ratas Wistar , Proteína Desacopladora 1/metabolismo
14.
J Pineal Res ; 45(4): 422-9, 2008 Nov.
Artículo en Inglés | MEDLINE | ID: mdl-18662218

RESUMEN

The aim of this work was to investigate the effect of the in vitro circadian-like exposure to melatonin [in the presence or absence of insulin (Ins)] on the metabolism and clock gene expression in adipocytes. To simulate the cyclic characteristics of the daily melatonin profile, isolated rat adipocytes were exposed in a circadian-like pattern to melatonin added to the incubating medium for 12 hr (mimicking the night), followed by an equal period without melatonin (mimicking the day) combined or not with Ins. This intermittent incubation was interrupted when four and a half 24-hr cycles were fulfilled. At the end, either during the induced night (melatonin present) or the induced day (melatonin absent), the rates of lipolysis and D-[U-(14)C]-glucose incorporation into lipids were estimated, in addition to the determination of lipogenic [glucose-6-phosphate dehydrogenase and fatty acid synthase (FAS)] and lipolytic (hormone sensitive lipase) enzymes and clock gene (Bmal-1b, Clock, Per-1 and Cry-1) mRNA expression. The leptin release was also measured. During the induced night, the following effects were observed: an increase in the mRNA expression of Clock, Per-1 and FAS; a rise in lipogenic response and leptin secretion; and a decrease in the lipolytic activity. The intermittent exposure of adipocytes to melatonin temporally and rhythmically synchronized their metabolic and hormonal function in a circadian fashion, mimicking what is observed in vivo in animals during the daily light-dark cycle. Therefore, this work helps to clarify the physiological relevance of the circadian pattern of melatonin secretion and its interactions with Ins, contributing to a better understanding of the adipocyte biology.


Asunto(s)
Adipocitos/metabolismo , Ritmo Circadiano , Regulación de la Expresión Génica , Melatonina/fisiología , Animales , Proteínas CLOCK , Proteínas de Ciclo Celular/genética , Proteínas de Ciclo Celular/metabolismo , Células Cultivadas , Criptocromos , Flavoproteínas/genética , Flavoproteínas/metabolismo , Glucosa/metabolismo , Insulina/fisiología , Leptina/metabolismo , Lipogénesis , Lipólisis , Masculino , Melatonina/administración & dosificación , Proteínas Circadianas Period , Radioinmunoensayo , Ratas , Ratas Wistar , Reacción en Cadena de la Polimerasa de Transcriptasa Inversa , Transactivadores/genética , Transactivadores/metabolismo
15.
Life Sci ; 82(1-2): 108-14, 2008 Jan 02.
Artículo en Inglés | MEDLINE | ID: mdl-18048060

RESUMEN

The mammalian pineal gland synthesizes melatonin in a circadian manner, peaking during the dark phase. This synthesis is primarily regulated by sympathetic innervations via noradrenergic fibers, but is also modulated by many peptidergic and hormonal systems. A growing number of studies reveal a complex role for melatonin in influencing various physiological processes, including modulation of insulin secretion and action. In contrast, a role for insulin as a modulator of melatonin synthesis has not been investigated previously. The aim of the current study was to determine whether insulin modulates norepinephrine (NE)-mediated melatonin synthesis. The results demonstrate that insulin (10(- 8)M) potentiated norepinephrine-mediated melatonin synthesis and tryptophan hydroxylase (TPOH) activity in ex vivo incubated pineal glands. When ex vivo incubated pineal glands were synchronized (12h NE-stimulation, followed by 12h incubation in the absence of NE), insulin potentiated NE-mediated melatonin synthesis and arylalkylamine-N-acetyltransferase (AANAT) activity. Insulin did not affect the activity of hydroxyindole-O-methyltranferase (HIOMT), nor the gene expression of tpoh, aanat, or hiomt, under any of the conditions investigated. We conclude that insulin potentiates NE-mediated melatonin synthesis in cultured rat pineal gland, potentially through post-transcriptional events.


Asunto(s)
Ritmo Circadiano/fisiología , Insulina/farmacología , Melatonina/biosíntesis , Norepinefrina/farmacología , Glándula Pineal/efectos de los fármacos , Acetilserotonina O-Metiltransferasa/genética , Acetilserotonina O-Metiltransferasa/metabolismo , Animales , N-Acetiltransferasa de Arilalquilamina/genética , N-Acetiltransferasa de Arilalquilamina/metabolismo , Expresión Génica/efectos de los fármacos , Técnicas In Vitro , Insulina/fisiología , Masculino , Norepinefrina/fisiología , Glándula Pineal/enzimología , Glándula Pineal/metabolismo , Procesamiento Proteico-Postraduccional , Ratas , Ratas Wistar , Reacción en Cadena de la Polimerasa de Transcriptasa Inversa , Triptófano Hidroxilasa/genética , Triptófano Hidroxilasa/metabolismo
16.
Interv Med Appl Sci ; 10(4): 226-232, 2018 Dec.
Artículo en Inglés | MEDLINE | ID: mdl-30792919

RESUMEN

BACKGROUND AND AIMS: The treatment with glucocorticoids may induce molecular changes in the level and/or degree of phosphorylation of proteins located downstream of the insulin receptor/insulin-like growth factor receptor (IR/IGF1R) in many tissues. However, few studies have investigated the intracellular insulin pathway in the masseter muscle. Therefore, this study aimed to analyze the IR/IGF1R signaling pathway in the masseter muscle of rats treated with dexamethasone. MATERIALS AND METHODS: Male Wistar rats were divided into two groups: control group (intraperitoneally injected with 0.9% NaCl solution) and dexamethasone group [intraperitoneally injected with 1 mg/kg (bw) dexamethasone solution] for 10 consecutive days. Sections of the masseter muscle were removed at time zero and after the infusion of regular insulin into the portal vein. RESULTS: Dexamethasone administration induces body weight loss without changing masseter muscle weight and reduces the expression of total IR and PI3K proteins; total levels of IRS1, Akt, and ERK1 remain unchanged between groups. The degree of phosphorylation/activity of IRS1 after insulin stimulus increased only in the control group; degree of phosphorylation of Akt increased in both groups, but this increase was attenuated in the dexamethasone group. DISCUSSION AND CONCLUSION: The degree of phosphorylation/activity in the masseter muscle is different from that in other muscle territories.

17.
Life Sci ; 199: 158-166, 2018 Apr 15.
Artículo en Inglés | MEDLINE | ID: mdl-29501522

RESUMEN

AIMS: Melatonin treatment has been reported to be capable of ameliorating metabolic diabetes-related abnormalities but also to cause hypogonadism in rats. We investigated whether the combined treatment with melatonin and insulin can improve insulin resistance and other metabolic disorders in rats with streptozotocin-induced diabetes during neonatal period and the repercussion of this treatment on the hypothalamic-pituitary-gonadal axis. MAIN METHODS: At the fourth week of age, diabetic animals started an 8-wk treatment with only melatonin (0.2 mg/kg body weight) added to drinking water at night or associated with insulin (NHP, 1.5 U/100 g/day) or only insulin. Animals were then euthanized, and the subcutaneous (SC), epididymal (EP), and retroperitoneal (RP) fat pads were excised, weighed and processed for adipocyte isolation for morphometric analysis as well as for measuring glucose uptake, oxidation, and incorporation of glucose into lipids. Hypothalamus was collected for gene expression and blood samples were collected for biochemical assays. KEY FINDINGS: The treatment with melatonin plus insulin (MI) was capable of maintaining glycemic control. In epididymal (EP) and subcutaneous (SC) adipocytes, the melatonin plus insulin (MI) treatment group recovered the insulin responsiveness. In the hypothalamus, melatonin treatment alone promoted a significant reduction in kisspeptin-1, neurokinin B and androgen receptor mRNA levels, in relation to control group. SIGNIFICANCE: Combined treatment with melatonin and insulin promoted a better glycemic control, improving insulin sensitivity in white adipose tissue (WAT). Indeed, melatonin treatment reduced hypothalamic genes related to reproductive function.


Asunto(s)
Tejido Adiposo Blanco/efectos de los fármacos , Glucemia/efectos de los fármacos , Diabetes Mellitus Experimental/tratamiento farmacológico , Insulina/administración & dosificación , Melatonina/administración & dosificación , Reproducción/efectos de los fármacos , Tejido Adiposo Blanco/metabolismo , Animales , Glucemia/metabolismo , Diabetes Mellitus Experimental/metabolismo , Quimioterapia Combinada , Índice Glucémico/efectos de los fármacos , Índice Glucémico/fisiología , Masculino , Ratas , Ratas Wistar , Reproducción/fisiología , Resultado del Tratamiento
18.
Nat Sci Sleep ; 10: 203-215, 2018.
Artículo en Inglés | MEDLINE | ID: mdl-30046256

RESUMEN

BACKGROUND: Melatonin is a neuroendocrine hormone that regulates many functions involving energy metabolism and behavior in mammals throughout the light/dark cycle. It is considered an output signal of the central circadian clock, located in the suprachiasmatic nucleus of the hypothalamus. Melatonin synthesis can be influenced by other hormones, such as insulin and glucocorticoids in pathological conditions or during stress. Furthermore, glucocorticoids appear to modulate circadian clock genes in peripheral tissues and are associated with the onset of metabolic diseases. In the pineal gland, the modulation of melatonin synthesis by clock genes has already been demonstrated. However, few studies have shown the effects of glucocorticoids on clock genes expression in the pineal gland. RESULTS: We verified that rats treated with dexamethasone (2 mg/kg body weight, intraperitoneal) for 10 consecutive days, showed hyperglycemia and pronounced hyperinsulinemia during the dark phase. Insulin sensitivity, glucose tolerance, melatonin synthesis, and enzymatic activity of arylalkylamine N-acetyltransferase, the key enzyme of melatonin synthesis, were reduced. Furthermore, we observed an increase in the expression of Bmal1, Per1, Per2, Cry1, and Cry2 in pineal glands of rats treated with dexamethasone. CONCLUSION: These results show that chronic treatment with dexamethasone can modulate both melatonin synthesis and circadian clock expression during the dark phase.

19.
Metabolism ; 56(7): 977-84, 2007 Jul.
Artículo en Inglés | MEDLINE | ID: mdl-17570261

RESUMEN

The use of experimental models of diabetes mellitus (DM) has been useful in understanding the complex pathogenesis of DM. Streptozotocin (STZ) injected in rats during the neonatal period has usually led to the major features described in diabetic patients (hyperglycemia, polyphagia, polydipsia, polyuria, and abnormal glucose tolerance) in a short period. Diabetes mellitus is a product of low insulin sensibility and pancreatic beta-cell dysfunction. Its process is characterized by a symptomless prediabetic phase before the development of the disease. In this study, we investigated the long-term effects of diabetes induction regarding the cellular metabolic aspects of this model and its similarities with diabetes found in humans. Male Wistar rats (5-day old) were intraperitoneally injected with STZ (150 mg/kg) and followed up for 12 weeks. On the 12th week, animals were decapitated and peri-epididymal fat pads were excised for adipocyte isolation. The following studies were performed: insulin-stimulated 2-deoxy-d-[(3)H]glucose uptake; incorporation of d-[U-(14)C]-glucose into lipids and conversion into (14)CO(2); and insulin binding. The weight gain rate of the STZ-treated group became significantly lower by the eighth week. These rats developed polyphagia, polydipsia, polyuria, and glycosuria, and impaired glucose tolerance. Biological tests with isolated adipocytes revealed a reduction in the insulin receptor number and an impairment in their ability to oxidize glucose as well as to incorporate it into lipids. Interestingly, parallel to reduced body weight, the adipocyte size of STZ rats was significantly small. We concluded that apart of a decrease in pancreatic insulin content, this experimental model of DM promotes a remarkable and sustained picture of insulin resistance in adulthood that is strongly related to a loss in adipose mass.


Asunto(s)
Tejido Adiposo/metabolismo , Diabetes Mellitus Experimental/metabolismo , Animales , Animales Recién Nacidos , Glucemia/análisis , Modelos Animales de Enfermedad , Glucosa/metabolismo , Prueba de Tolerancia a la Glucosa , Insulina/metabolismo , Resistencia a la Insulina , Masculino , Ratas , Ratas Wistar , Estreptozocina
20.
J Pediatr (Rio J) ; 83(5 Suppl): S192-203, 2007 Nov.
Artículo en Inglés | MEDLINE | ID: mdl-17989837

RESUMEN

OBJECTIVE: To describe the advances in research into the physiological role of white adipose tissue, with emphasis on its endocrinal role in inflammatory processes, feeding behavior, insulin sensitization and modulation of the atherogenetic process. To deal with the potential role of adipose tissue as a source of stem cells for regeneration of tissues, with special emphasis on adipogenesis and its consequences for development of obesity. SOURCES: Important information was compiled from the scientific literature in order that this analysis contains an explanatory synthesis of the aspects mentioned above. SUMMARY OF THE FINDINGS In addition to its classical functions as primary metabolic energy store, meeting energy requirements during periods of deprivation by means of lypolisis, adipose tissue also has the capacity to synthesize and secrete a variety of hormones - the adipokines. These are active in a range of processes, such as control of nutritional intake (leptin) and control of sensitivity to insulin and inflammatory processes (TNF-alpha, IL-6, resistin, visfatin, adiponectin). Furthermore, since adipose tissue also contains undifferentiated cells, it has the ability to generate new adipocytes, regenerating its own tissue (adipogenesis), and also the ability to give rise to other cells (myoblasts, chondroblasts, osteoblasts), which has great therapeutic potential in the not-too-distant future. CONCLUSIONS: The range of functional possibilities of adipose tissue has widened. An understanding of these potentials could make this tissue a great ally in the fight against conditions that are currently assuming epidemic proportions (obesity, diabetes mellitus, arterial hypertension and arteriosclerosis) and in which adipose tissue is still seen as the enemy.


Asunto(s)
Adipocitos/metabolismo , Tejido Adiposo/metabolismo , Enfermedades Cardiovasculares/metabolismo , Glándulas Endocrinas/metabolismo , Adipocitos/patología , Adipogénesis/fisiología , Adipoquinas/metabolismo , Tejido Adiposo/patología , Tejido Adiposo Pardo , Tejido Adiposo Blanco/metabolismo , Tejido Adiposo Blanco/patología , Enfermedades Cardiovasculares/patología , Diabetes Mellitus/metabolismo , Glándulas Endocrinas/patología , Humanos , Inflamación/metabolismo , Inflamación/patología , Lipogénesis/fisiología , Lipólisis/fisiología , Obesidad/metabolismo
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