Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 20 de 143
Filtrar
1.
Nutrients ; 13(7)2021 Jun 24.
Artigo em Inglês | MEDLINE | ID: mdl-34202894

RESUMO

Consumption of different types of high-calorie foods leads to the development of various metabolic disorders. However, the effects of multi-strain probiotics on different types of diet-induced obesity and intestinal dysbiosis remain unclear. In this study, mice were fed a control diet, high-fat diet (HFD; 60% kcal fat and 20% kcal carbohydrate), or western diet (WD; 40% kcal fat and 43% kcal carbohydrate) and administered with multi-strain AB-Kefir containing six strains of lactic acid bacteria and a Bifidobacterium strain, at 109 CFU per mouse for 10 weeks. Results demonstrated that AB-Kefir reduced body weight gain, glucose intolerance, and hepatic steatosis with a minor influence on gut microbiota composition in HFD-fed mice, but not in WD-fed mice. In addition, AB-Kefir significantly reduced the weight and size of adipose tissues by regulating the expression of CD36, Igf1, and Pgc1 in HFD-fed mice. Although AB-Kefir did not reduce the volume of white adipose tissue, it markedly regulated CD36, Dgat1 and Mogat1 mRNA expression. Moreover, the abundance of Eubacterium_coprostanoligenes_group and Ruminiclostridium significantly correlated with changes in body weight, liver weight, and fasting glucose in test mice. Overall, this study provides important evidence to understand the interactions between probiotics, gut microbiota, and diet in obesity treatment.


Assuntos
Dieta da Carga de Carboidratos/métodos , Dieta Hiperlipídica/métodos , Kefir/microbiologia , Obesidade/dietoterapia , Probióticos/administração & dosagem , Tecido Adiposo/efeitos dos fármacos , Animais , Peso Corporal , Dieta da Carga de Carboidratos/efeitos adversos , Dieta Hiperlipídica/efeitos adversos , Dieta Ocidental , Sacarose na Dieta/administração & dosagem , Modelos Animais de Doenças , Disbiose/dietoterapia , Disbiose/microbiologia , Fígado Gorduroso/dietoterapia , Fígado Gorduroso/microbiologia , Microbioma Gastrointestinal/efeitos dos fármacos , Intolerância à Glucose/dietoterapia , Intolerância à Glucose/microbiologia , Inflamação , Fígado/patologia , Camundongos , Camundongos Obesos , Obesidade/etiologia , Obesidade/microbiologia , Ganho de Peso/efeitos dos fármacos
2.
Nutrients ; 13(6)2021 Jun 05.
Artigo em Inglês | MEDLINE | ID: mdl-34198888

RESUMO

BACKGROUND: Foods rich in saturated fatty acids (SFAs) have been discouraged by virtue of their cholesterol-raising potential, but this effect is modulated by the food source and background level of carbohydrate. OBJECTIVE: We aimed to compare the consumption of palm stearin (PS) versus butter on circulating cholesterol responses in the setting of both a low-carbohydrate/high-fat (LC/HF) and high-carbohydrate/low-fat (HC/LF) diet in healthy subjects. We also explored effects on plasma lipoprotein particle distribution and fatty acid composition. METHODS: We performed a randomized, controlled-feeding, cross-over study that compared a PS- versus a Butter-based diet in a group of normocholesterolemic, non-obese adults. A controlled canola oil-based 'Run-In' diet preceded the experimental PS and Butter diets. All diets were eucaloric, provided for 3-weeks, and had the same macronutrient distribution but varied in primary fat source (40% of the total fat). The same Run-In and cross-over experiments were done in two separate groups who self-selected to either a LC/HF (n = 12) or a HC/LF (n = 12) diet track. The primary outcomes were low-density lipoprotein-cholesterol (LDL-C), high-density lipoprotein (HDL)-C, triglycerides, and LDL particle distribution. RESULTS: Compared to PS, Butter resulted in higher LDL-C in both the LC/HF (13.4%, p = 0.003) and HC/LF (10.8%, p = 0.002) groups, which was primarily attributed to large LDL I and LDL IIa particles. There were no differences between PS and Butter in HDL-C, triglycerides, or small LDL particles. Oxidized LDL was lower after PS than Butter in LC/HF (p = 0.011), but not the HC/LF group. CONCLUSIONS: These results demonstrate that Butter raises LDL-C relative to PS in healthy normocholesterolemic adults regardless of background variations in carbohydrate and fat, an effect primarily attributed to larger cholesterol-rich LDL particles.


Assuntos
Manteiga , Colesterol/sangue , Dieta/métodos , Carboidratos da Dieta/administração & dosagem , Gorduras na Dieta/administração & dosagem , Óleo de Palmeira/administração & dosagem , Adulto , Idoso , Estudos Cross-Over , Dieta/efeitos adversos , Dieta da Carga de Carboidratos/efeitos adversos , Dieta da Carga de Carboidratos/métodos , Dieta com Restrição de Carboidratos/efeitos adversos , Dieta com Restrição de Carboidratos/métodos , Dieta com Restrição de Gorduras/efeitos adversos , Dieta com Restrição de Gorduras/métodos , Dieta Hiperlipídica/efeitos adversos , Dieta Hiperlipídica/métodos , Feminino , Voluntários Saudáveis , Humanos , Lipídeos/sangue , Masculino , Pessoa de Meia-Idade , Óleo de Palmeira/química , Adulto Jovem
3.
Artigo em Inglês | MEDLINE | ID: mdl-34192612

RESUMO

Type 2 Diabetes mellitus (T2DM) is a multifactorial and polygenic disorder with the molecular bases still idiopathic. Experimental analyses and tests are quite limited upon human samples due to the access, variability of patient's conditions, and the size and complexity of the genome. Therefore, high-sugar diet exposure is commonly used for modeling T2DM in non-human animals, which includes invertebrate organisms like the fruit fly Drosophila melanogaster. Interestingly, high-sugar diet (HSD) induces delayed time for pupation and reduced viability in fruit fly larvae hatched from a 30% sucrose-containing medium (HSD-30%). Here we carried out an mRNA-deep sequencing study to identify differentially transcribed genes in adult fruit fly hatched and reared from an HSD-30%. Seven days after hatching, flies reared on control and HSD-30% were used to glucose and triglyceride level measurements and RNA extraction for sequencing. Remarkably, glucose levels were about 2-fold higher than the control group in fruit flies exposed to HSD-30%, whereas triglycerides levels increased 1.7-fold. After RNA-sequencing, we found that 13.5% of the genes were differentially transcribed in the dyslipidemic and hyperglycaemic insects. HSD-30% up-regulated genes involved in ribosomal biogenesis (e.g. dTOR, ERK and dS6K) and down-regulated genes involved in energetic process (e.g. Pfk, Gapdh1, and Pyk from pyruvate metabolism; kdn, Idh and Mdh2 from the citric acid cycle; ATPsynC and ATPsynẞ from ATP synthesis) and insect development. We found a remarkable down-regulation for Actin (Act88F) that likely impairs muscle development. Moreover, HSD-30% up-regulated both the insulin-like peptides 7 and 8 and down-regulated the insulin receptor substrate p53, isoform A and insulin-like peptide 6 genes, whose functional products are insulin signaling markers. All these features pointed together to a tightly correlation of the T2DM-like phenotype modeled by the D. melanogaster and an intricate array of phenomena, which includes energetic processes, muscle development, and ribosomal synthesis as that observed for the human pathology.


Assuntos
Diabetes Mellitus Experimental/genética , Diabetes Mellitus Tipo 2/genética , Dieta da Carga de Carboidratos/efeitos adversos , Açúcares da Dieta/efeitos adversos , Drosophila melanogaster/genética , Transcriptoma/efeitos dos fármacos , Animais , Diabetes Mellitus Experimental/metabolismo , Diabetes Mellitus Experimental/patologia , Diabetes Mellitus Tipo 2/metabolismo , Diabetes Mellitus Tipo 2/patologia , Drosophila melanogaster/efeitos dos fármacos , Drosophila melanogaster/metabolismo , Regulação da Expressão Gênica , Glucose/análise , Humanos , Estresse Oxidativo , Triglicerídeos/metabolismo
4.
Nutrients ; 13(5)2021 May 06.
Artigo em Inglês | MEDLINE | ID: mdl-34066330

RESUMO

Consumption of fructose has been associated with a higher risk of developing obesity and metabolic syndrome (MetS). The aim of this study was to examine the long-term effects of fructose compared to starch from high-amylose maize starch (HiMaize) at ad libitum feeding in a juvenile Göttingen Minipig model with 20% of the diet provided as fructose as a high-risk diet (HR, n = 15) and 20% as HiMaize as a lower-risk control diet (LR, n = 15). The intake of metabolizable energy was on average similar (p = 0.11) among diets despite increased levels of the satiety hormone PYY measured in plasma (p = 0.0005) of the LR pigs. However, after over 20 weeks of ad libitum feeding, no difference between diets was observed in daily weight gain (p = 0.103), and a difference in BW was observed only at the end of the experiment. The ad libitum feeding promoted an obese phenotype over time in both groups with increased plasma levels of glucose (p = 0.005), fructosamine (p < 0.001), insulin (p = 0.03), and HOMA-IR (p = 0.02), whereas the clinical markers of dyslipidemia were unaffected. When compared to the LR diet, fructose did not accelerate the progression of MetS associated parameters and largely failed to change markers that indicate a stimulated de novo lipogenesis.


Assuntos
Dieta da Carga de Carboidratos/efeitos adversos , Ingestão de Energia/fisiologia , Frutose/administração & dosagem , Síndrome Metabólica/etiologia , Obesidade/etiologia , Animais , Biomarcadores/sangue , Dieta da Carga de Carboidratos/métodos , Modelos Animais de Doenças , Dislipidemias/sangue , Metabolismo Energético/fisiologia , Amido/administração & dosagem , Suínos , Porco Miniatura , Ganho de Peso/efeitos dos fármacos , Zea mays
5.
Nutrients ; 13(5)2021 May 20.
Artigo em Inglês | MEDLINE | ID: mdl-34065444

RESUMO

Resveratrol and its 2-methoxy derivative pterostilbene are two phenolic compounds that occur in foodstuffs and feature hepato-protective effects. This study is devoted to analysing and comparing the metabolic effects of pterostilbene and resveratrol on gut microbiota composition in rats displaying NAFLD induced by a diet rich in saturated fat and fructose. The associations among changes induced by both phenolic compounds in liver status and those induced in gut microbiota composition were also analysed. For this purpose, fifty Wistar rats were distributed in five experimental groups: a group of animals fed a standard diet (CC group) and four additional groups fed a high-fat high-fructose diet alone (HFHF group) or supplemented with 15 or 30 mg/kg bw/d of pterostilbene (PT15 and PT30 groups, respectively) or 30 mg/kg bw/d of resveratrol (RSV30 group). The dramatic changes induced by high-fat high-fructose feeding in the gut microbiota were poorly ameliorated by pterostilbene or resveratrol. These results suggest that the specific changes in microbiota composition induced by pterostilbene (increased abundances of Akkermansia and Erysipelatoclostridium, and lowered abundance of Clostridum sensu stricto 1) may not entirely explain the putative preventive effects on steatohepatitis.


Assuntos
Microbioma Gastrointestinal/efeitos dos fármacos , Hepatopatia Gordurosa não Alcoólica/tratamento farmacológico , Resveratrol/farmacologia , Estilbenos/farmacologia , Animais , Dieta da Carga de Carboidratos/efeitos adversos , Dieta Hiperlipídica/efeitos adversos , Gorduras na Dieta/administração & dosagem , Frutose/administração & dosagem , Masculino , Hepatopatia Gordurosa não Alcoólica/etiologia , Hepatopatia Gordurosa não Alcoólica/microbiologia , Ratos , Ratos Wistar
6.
Nutrients ; 13(4)2021 Apr 19.
Artigo em Inglês | MEDLINE | ID: mdl-33921866

RESUMO

Persistence of damage induced by unhealthy diets during youth has been little addressed. Therefore, we investigated the impact of a short-term fructose-rich diet on liver metabolic activity in adolescent rats and the putative persistence of alterations after removing fructose from the diet. Adolescent rats were fed a fructose-rich diet for three weeks and then switched to a control diet for further three weeks. Body composition and energy balance were not affected by fructose-rich diet, while increased body lipids and lipid gain were found after the rescue period. Switching to a control diet reversed the upregulation of plasma fructose, uric acid, lipocalin, and haptoglobin, while plasma triglycerides, alanine aminotransferase, lipopolysaccharide, and tumor necrosis factor alpha remained higher. Hepatic steatosis and ceramide were increased by fructose-rich diet, but reversed by returning to a control diet, while altered hepatic response to insulin persisted. Liver fatty acid synthase and stearoyl-CoA desaturase (SCD) activities were upregulated by fructose-rich diet, and SCD activity remained higher after returning to the control diet. Fructose-induced upregulation of complex II-driven mitochondrial respiration, peroxisome proliferator-activated receptor-gamma coactivator 1 alpha, and peroxisome proliferator activated receptor α also persisted after switching to control diet. In conclusion, our results show prolonged fructose-induced dysregulation of liver metabolic activity.


Assuntos
Dieta da Carga de Carboidratos/efeitos adversos , Ingestão de Alimentos/fisiologia , Frutose/administração & dosagem , Resistência à Insulina/fisiologia , Mitocôndrias/metabolismo , Alanina Transaminase/sangue , Animais , Composição Corporal , Ceramidas/metabolismo , Modelos Animais de Doenças , Metabolismo Energético , Fígado Gorduroso/etiologia , Frutose/sangue , Haptoglobinas/metabolismo , Lipídeos/sangue , Lipocalinas/sangue , Lipopolissacarídeos/sangue , Fígado/metabolismo , Ratos , Triglicerídeos/sangue , Fator de Necrose Tumoral alfa/sangue , Regulação para Cima/fisiologia , Ácido Úrico/sangue
7.
J Nutr Biochem ; 92: 108622, 2021 06.
Artigo em Inglês | MEDLINE | ID: mdl-33705942

RESUMO

The high prevalence of obesity and associated metabolic disorders are one of the major public health problems worldwide. Among the main causal factors of obesity, excessive consumption of food rich in sugar and fat stands out due to its high energy density. The regulation of food intake relies on hypothalamic control by the action of several neuropeptides. Excessive consumption of hypercaloric diets has impact in the behavior and in the gut microbiota. In the present study, we used a high-sugar and fat (HSB) diet for 12 weeks to induce obesity in C57BL/6 mice and to investigate its effects on the gut microbiota, hypothalamic peptides, and behavior. We hypothesize that chronic consumption of HSB diet can change the behavior. Additionally, we also hypothesize that changes in gut microbiota can be associated with changes in the transcriptional regulation of hypothalamic peptides and behavior. To evaluate the gut microbiota, we performed the sequencing of 16S rRNA gene, which demonstrate that HSB diet modulates the gut microbiota with an increase in the Firmicutes and Actinobacteria phylum and a decrease of Bacteroidetes phylum. The real time qPCR revealed that HSB-fed mice presented changes in the transcriptional regulation of hypothalamic neuropeptides genes such as Npy, Gal and Galr1. The Marble-burying and Light/dark box tests also showed an alteration in anxiety and impulsive behaviors for the HSB-fed mice. Our data provides evidence that obesity induced by HSB diet consumption is associated with alterations in gut microbiota and behavior, highlighting the multifactorial characteristics of this disease.


Assuntos
Dieta da Carga de Carboidratos/efeitos adversos , Dieta Hiperlipídica/efeitos adversos , Microbioma Gastrointestinal , Obesidade/etiologia , Obesidade/microbiologia , Actinobacteria/genética , Actinobacteria/isolamento & purificação , Animais , Bacteroidetes/genética , Bacteroidetes/isolamento & purificação , Firmicutes/genética , Firmicutes/isolamento & purificação , Masculino , Camundongos Endogâmicos C57BL
8.
Int J Mol Sci ; 22(5)2021 Feb 28.
Artigo em Inglês | MEDLINE | ID: mdl-33670975

RESUMO

Excessive intake of fructose results in metabolic syndrome (MS) and kidney damage, partly mediated by its metabolism by fructokinase-C or ketohexokinase-C (KHK-C). Osthol has antioxidant properties, is capable of regulating adipogenesis, and inhibits KHK-C activity. Here, we examined the potential protective role of osthol in the development of kidney disease induced by a Western (high-fat/high-sugar) diet. Control rats fed with a high-fat/high-sugar diet were compared with two groups that also received two different doses of osthol (30 mg/kg/d or 40 mg/kg/d body weight BW). A fourth group served as a normal control and received regular chow. At the end of the follow-up, kidney function, metabolic markers, oxidative stress, and lipogenic enzymes were evaluated. The Western diet induced MS (hypertension, hyperglycemia, hypertriglyceridemia, obesity, hyperuricemia), a fall in the glomerular filtration rate, renal tubular damage, and increased oxidative stress in the kidney cortex, with increased expression of lipogenic enzymes and increased kidney KHK expression. Osthol treatment prevented the development of MS and ameliorated kidney damage by inhibiting KHK activity, preventing oxidative stress via nuclear factor erythroid 2-related factor (Nrf2) activation, and reducing renal lipotoxicity. These data suggest that the nutraceutical osthol might be an ancillary therapy to slow the progression of MS and kidney damage induced by a Western diet.


Assuntos
Cumarínicos/farmacologia , Dieta Ocidental/efeitos adversos , Frutoquinases/antagonistas & inibidores , Nefropatias/prevenção & controle , Síndrome Metabólica/prevenção & controle , Animais , Cumarínicos/uso terapêutico , Dieta da Carga de Carboidratos/efeitos adversos , Dieta Hiperlipídica/efeitos adversos , Frutoquinases/metabolismo , Frutose/metabolismo , Nefropatias/etiologia , Nefropatias/metabolismo , Masculino , Síndrome Metabólica/etiologia , Síndrome Metabólica/metabolismo , Fator 2 Relacionado a NF-E2 , Estresse Oxidativo , Substâncias Protetoras/farmacologia , Substâncias Protetoras/uso terapêutico , Ratos , Ratos Wistar
9.
Biochem Biophys Res Commun ; 534: 533-539, 2021 01 01.
Artigo em Inglês | MEDLINE | ID: mdl-33261883

RESUMO

OBJECTIVE: To investigate the effect of high fat diet-induced insulin resistance on autophagy markers in the liver and skeletal muscle of mice in the fasted state and following an oral glucose bolus. METHODS: Forty C57BL/6J male mice were fed either a high fat, high sucrose (HFSD, n = 20) or standard chow control (CON, n = 20) diet for 16 weeks. Upon trial completion, mice were gavaged with water or glucose and skeletal muscle and liver were collected 15 min post gavage. Protein abundance and gene expression of autophagy markers and activation of related signalling pathways were assessed. RESULTS: Compared to CON, the HFSD intervention increased LC3B-II and p62/SQSTM1 protein abundance in the liver which is indicative of elevated autophagosome content via reduced clearance. These changes coincided with inhibitory autophagy signalling through elevated p-mTOR S2448 and p-ULK1S758. HFSD did not alter autophagy markers in skeletal muscle. Administration of an oral glucose bolus had no effect on autophagy markers or upstream signalling responses in either tissue regardless of diet. CONCLUSION: HFSD induces tissue-specific autophagy impairments, with autophagosome accumulation indicating reduced lysosomal clearance in the liver. In contrast, autophagy markers were unchanged in skeletal muscle, indicating that autophagy is not involved in the development of skeletal muscle insulin resistance.


Assuntos
Autofagia , Resistência à Insulina , Metabolismo dos Lipídeos , Músculo Esquelético/metabolismo , Animais , Dieta da Carga de Carboidratos/efeitos adversos , Dieta Hiperlipídica/efeitos adversos , Fígado/metabolismo , Masculino , Camundongos Endogâmicos C57BL
10.
J Nutr Biochem ; 87: 108519, 2021 01.
Artigo em Inglês | MEDLINE | ID: mdl-33017610

RESUMO

Dietary sugar is an important determinant of the development and progression of nonalcoholic fatty liver disease (NAFLD). However, the molecular mechanisms underlying the deleterious effects of sugar intake on NAFLD under energy-balanced conditions are still poorly understood. Here, we provide a comprehensive analysis of the liver lipidome and mechanistic insights into the pathogenesis of NAFLD induced by the chronic consumption of high-sugar diet (HSD). Newly weaned male Wistar rats were fed either a standard chow diet or an isocaloric HSD for 18 weeks. Livers were harvested for histological, oxidative stress, gene expression, and lipidomic analyses. Intake of HSD increased oxidative stress and induced severe liver injury, microvesicular steatosis, and ballooning degeneration of hepatocytes. Using untargeted lipidomics, we identified and quantified 362 lipid species in the liver. Rats fed with HSD displayed increased hepatic levels of triacylglycerol enriched in saturated and monounsaturated fatty acids, lipids related to mitochondrial function/structure (phosphatidylglycerol, cardiolipin, and ubiquinone), and acylcarnitine (an intermediate lipid of fatty acid beta-oxidation). HSD-fed animals also presented increased levels of some species of membrane lipids and a decreased content of phospholipids containing omega-6 fatty acids. These changes in the lipidome were associated with the downregulation of genes involved in fatty acid oxidation in the liver. In conclusion, our data suggest that the chronic intake of a HSD, even under isocaloric conditions, induces lipid overload, and inefficient/impaired fatty acid oxidation in the liver. Such events lead to marked disturbance in hepatic lipid metabolism and the development of NAFLD.


Assuntos
Dieta da Carga de Carboidratos/efeitos adversos , Metabolismo dos Lipídeos , Fígado/metabolismo , Hepatopatia Gordurosa não Alcoólica/etiologia , Hepatopatia Gordurosa não Alcoólica/metabolismo , Animais , Lipidômica , Masculino , Redes e Vias Metabólicas , Ratos Wistar
11.
Nutrients ; 12(12)2020 Dec 07.
Artigo em Inglês | MEDLINE | ID: mdl-33297496

RESUMO

BACKGROUND: Increased dietary fructose consumption is closely associated with lipid and glucose metabolic disorders. Sasa quelpaertensis Nakai possesses various health-promoting properties, but there has been no research on its protective effect against fructose-induced metabolic dysfunction. In this study, we investigated the effects of S. quelpaertensis leaf extract (SQE) on metabolic dysfunction in high-fructose-diet-fed rats. METHODS: Animals were fed a 46% carbohydrate diet, a 60% high-fructose diet, or a 60% high-fructose diet with SQE (500 mg/kg of body weight (BW)/day) in drinking water for 16 weeks. Serum biochemical parameters were measured and the effects of SQE on hepatic histology, protein expression, and transcriptome profiles were investigated. RESULTS: SQE improved dyslipidemia and insulin resistance induced in high-fructose-diet-fed rats. SQE ameliorated the lipid accumulation and inflammatory response in liver tissues by modulating the expressions of key proteins related to lipid metabolism and antioxidant response. SQE significantly enriched the genes related to the metabolic pathway, namely, the tumor necrosis factor (TNF) signaling pathway and the PI3K-Akt signaling pathway. CONCLUSIONS: SQE could effectively prevent dyslipidemia, insulin resistance, and hepatic lipid accumulation by regulation of metabolism-related gene expressions, suggesting its role as a functional ingredient to prevent lifestyle-related metabolic disorders.


Assuntos
Dislipidemias/prevenção & controle , Resistência à Insulina/fisiologia , Metabolismo dos Lipídeos/efeitos dos fármacos , Extratos Vegetais/farmacologia , Sasa/química , Animais , Antioxidantes/farmacologia , Dieta da Carga de Carboidratos/efeitos adversos , Modelos Animais de Doenças , Dislipidemias/etiologia , Frutose/administração & dosagem , Fígado/metabolismo , Masculino , Ratos , Ratos Sprague-Dawley
12.
Nutrients ; 12(11)2020 Nov 20.
Artigo em Inglês | MEDLINE | ID: mdl-33233570

RESUMO

Aim: The objective of this study was to characterize the early effects of high fructose diets (with and without high fat) on both the composition of the gut microbiota and lipid metabolism in Syrian hamsters, a reproducible preclinical model of diet-induced dyslipidemia. Methods: Eight-week-old male hamsters were fed diets consisting of high-fat/high-fructose, low-fat/high-fructose or a standard chow diet for 14 days. Stool was collected at baseline (day 0), day 7 and day 14. Fasting levels of plasma triglycerides and cholesterol were monitored on day 0, day 7 and day 14, and nonfasting levels were also assayed on day 15. Then, 16S rRNA sequencing of stool samples was used to determine gut microbial composition, and predictive metagenomics was performed to evaluate dietary-induced shifts in deduced microbial functions. Results: Both high-fructose diets resulted in divergent gut microbiota composition. A high-fat/high-fructose diet induced the largest shift in overall gut microbial composition, with dramatic shifts in the Firmicute/Bacteroidetes ratio, and changes in beta diversity after just seven days of dietary intervention. Significant associations between genus level taxa and dietary intervention were identified, including an association with Ruminococceace NK4A214 group in high-fat/high-fructose fed animals and an association with Butryimonas with the low-fat/high-fructose diet. High-fat/high-fructose feeding induced dyslipidemia with increases in plasma triglycerides and cholesterol, and hepatomegaly. Dietary-induced changes in several genus level taxa significantly correlated with lipid levels over the two-week period. Differences in microbial metabolic pathways between high-fat/high-fructose and low-fat/high-fructose diet fed hamsters were identified, and several of these pathways also correlated with lipid profiles in hamsters. Conclusions: The high-fat/high-fructose diet caused shifts in the host gut microbiota. These dietary-induced alterations in gut microbial composition were linked to changes in the production of secondary metabolites, which contributed to the development of metabolic syndrome in the host.


Assuntos
Dieta da Carga de Carboidratos/efeitos adversos , Dieta Hiperlipídica/efeitos adversos , Dislipidemias , Frutose/farmacologia , Microbioma Gastrointestinal/efeitos dos fármacos , Animais , Bactérias/classificação , Bactérias/genética , Colesterol/sangue , Fezes/microbiologia , Metabolismo dos Lipídeos , Masculino , Mesocricetus , Metagenômica , RNA Ribossômico 16S/genética , Triglicerídeos/sangue
13.
Int J Mol Sci ; 21(21)2020 Oct 31.
Artigo em Inglês | MEDLINE | ID: mdl-33142948

RESUMO

Although feed cost is the greatest concern in aquaculture, the inclusion of carbohydrates in the fish diet, and their assimilation, are still not well understood in aquaculture species. We identified molecular events that occur due to the inclusion of high carbohydrate levels in the diets of genetically improved 'Jayanti rohu' Labeo rohita. To reveal transcriptional changes in the liver of rohu, a feeding experiment was conducted with three doses of gelatinized starch (20% (control), 40%, and 60%). Transcriptome sequencing revealed totals of 15,232 (4464 up- and 4343 down-regulated) and 15,360 (4478 up- and 4171 down-regulated) differentially expressed genes. Up-regulated transcripts associated with glucose metabolisms, such as hexokinase, PHK, glycogen synthase and PGK, were found in fish fed diets with high starch levels. Interestingly, a de novo lipogenesis mechanism was found to be enriched in the livers of treated fish due to up-regulated transcripts such as FAS, ACCα, and PPARγ. The insulin signaling pathways with enriched PPAR and mTOR were identified by Kyoto Encyclopedia of Genes and Genome (KEGG) as a result of high carbohydrates. This work revealed for the first time the atypical regulation transcripts associated with glucose metabolism and lipogenesis in the livers of Jayanti rohu due to the inclusion of high carbohydrate levels in the diet. This study also encourages the exploration of early nutritional programming for enhancing glucose efficiency in carp species, for sustainable and cost-effective aquaculture production.


Assuntos
Animais Geneticamente Modificados/metabolismo , Carpas/metabolismo , Dieta da Carga de Carboidratos/efeitos adversos , Fígado/metabolismo , Análise de Sequência de RNA/métodos , Animais , Animais Geneticamente Modificados/genética , Aquicultura/métodos , Metabolismo dos Carboidratos , Carpas/genética , Regulação da Expressão Gênica , Fígado/patologia , Transdução de Sinais , Transcriptoma
14.
J Nutr Biochem ; 85: 108463, 2020 11.
Artigo em Inglês | MEDLINE | ID: mdl-32891893

RESUMO

The objective of this study was to develop a well-characterized mouse model of nonalcoholic steatohepatitis (NASH) with a strong manifestation of liver fibrosis. The progression of metabolic, inflammatory and fibrotic features of this mouse model was monitored by performing in vivo time-course study. Male C57BL/6J mice were fed a high-fat/high-sucrose/high-cholesterol diet (34% fat, 34% sucrose and 2.0% cholesterol, by weight) for 2, 4, 6, 8, 10, 12, 14 or 16 weeks to induce obesity-associated metabolic dysfunctions, inflammation and fibrosis in the liver and white adipose tissue (WAT). Body and liver weights were gradually increased with significant hepatic triglyceride accumulation, i.e., liver steatosis, and marked elevation of serum alanine transaminase levels at week 10. While hepatic inflammation was displayed with the highest expression of macrophage markers and M1 markers at week 6, liver fibrosis determined by collagen accumulation was continuously increased to week 16. In epididymal WAT, weights and adipocyte size peaked at week 6-8. The increased expression of fibrogenic genes preceded inflammatory features (week 2 to 6 vs. week 6 to 16), suggesting that early fibrosis may trigger inflammatory events in the WAT. This study established a mouse model of diet-induced NASH with a strong manifestation of liver fibrosis. This mouse model will be a valuable in vivo tool in studying the pathophysiology of NASH and also in testing preventive and therapeutic potentials of dietary components and drugs against NASH with liver fibrosis.


Assuntos
Inflamação/metabolismo , Cirrose Hepática/metabolismo , Fígado/patologia , Hepatopatia Gordurosa não Alcoólica/metabolismo , Animais , Dieta da Carga de Carboidratos/efeitos adversos , Dieta Hiperlipídica/efeitos adversos , Modelos Animais de Doenças , Inflamação/etiologia , Inflamação/patologia , Fígado/metabolismo , Cirrose Hepática/etiologia , Cirrose Hepática/patologia , Masculino , Camundongos Endogâmicos C57BL , Hepatopatia Gordurosa não Alcoólica/complicações , Hepatopatia Gordurosa não Alcoólica/etiologia , Hepatopatia Gordurosa não Alcoólica/patologia
15.
Mol Med Rep ; 22(4): 2860-2868, 2020 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-32945408

RESUMO

Hydrogen exhibits therapeutic and preventive effects against various diseases. The present study investigated the potential protective effect and dose­dependent manner of hydrogen inhalation on high fat and fructose diet (HFFD)­induced nonalcoholic fatty liver disease (NAFLD) in Sprague­Dawley rats. Rats were randomly divided into four groups: i) Control group, regular diet/air inhalation; ii) model group, HFFD/air inhalation; iii) low hydrogen group, HFFD/4% hydrogen inhalation; and iv) high hydrogen group, HFFD/67% hydrogen inhalation. After a 10­week experiment, hydrogen inhalation ameliorated weight gain, abdominal fat index, liver index and body mass index of rats fed with HFFD and lowered the total area under the curve in an oral glucose tolerance test. Hydrogen inhalation also ameliorated the increase in liver lipid content and alanine transaminase and aspartate transaminase activities. Liver histopathologic changes evaluated with hematoxylin and eosin as well as Oil Red O staining revealed lower lipid deposition in hydrogen inhalation groups, consistent with the decrease in the expression of the lipid synthesis gene SREBP­1c. The majority of the indicators were affected following treatment with hydrogen in a dose­dependent manner. In conclusion, hydrogen inhalation may play a protective role by influencing the general state, lipid metabolism parameters, liver histology and liver function indicators in the rat model of metabolic syndrome with NAFLD.


Assuntos
Hidrogênio/administração & dosagem , Síndrome Metabólica/complicações , Hepatopatia Gordurosa não Alcoólica/complicações , Hepatopatia Gordurosa não Alcoólica/tratamento farmacológico , Substâncias Protetoras/administração & dosagem , Administração por Inalação , Animais , Índice de Massa Corporal , Dieta da Carga de Carboidratos/efeitos adversos , Dieta Hiperlipídica/efeitos adversos , Modelos Animais de Doenças , Relação Dose-Resposta a Droga , Teste de Tolerância a Glucose , Metabolismo dos Lipídeos/efeitos dos fármacos , Fígado/efeitos dos fármacos , Fígado/metabolismo , Masculino , Hepatopatia Gordurosa não Alcoólica/etiologia , Ratos , Ratos Sprague-Dawley , Ganho de Peso/efeitos dos fármacos
16.
Sci Rep ; 10(1): 15048, 2020 09 14.
Artigo em Inglês | MEDLINE | ID: mdl-32929110

RESUMO

Changes associated with cognitive function in the high-fat high-carbohydrate diet-induced prediabetes animal model and effect of exercise remain unclear. Rats were randomly assigned to the following groups (n = 6): non-diabetic (ND), prediabetic (PD), intermittent exercising PD (PD + IE) and regular exercising PD (PD + RE). After exercise cessation, oral glucose tolerance (OGT), Novel Object Recognition Test (NORT) and Morris-Water Maze (MWM) tests were performed to assess cognitive function. After sacrifice, malonaldehyde, glutathione peroxidase, interleukin-1ß and dopamine concentration in the prefrontal cortex (PFC) and hippocampus were measured. Impaired OGT response in PD animals was accompanied by poor performance on behavioural tasks. This was associated with increased oxidative stress markers and impaired dopamine neurotransmission as evidence by elevated dopamine concentration in the PFC and hippocampal tissue. Improved OGT response by exercise was coupled with improved performance on behavioural tasks, oxidative stress markers and increased interleukin-1ß concentration. In regular exercise, this was further coupled with improved dopamine neurotransmission. Cognitive function was affected during prediabetes in animals. This was partly due to oxidative stress and impaired dopamine neurotransmission. Both intermittent and regular exercise improved cognitive function. This was partly mediated by improved glucose tolerance and oxidative stress as well as a subclinical increase in interleukin-1ß concentration. In regular exercise, this was further mediated by improved dopamine neurotransmission.


Assuntos
Cognição , Memória , Condicionamento Físico Animal/métodos , Estado Pré-Diabético/fisiopatologia , Aprendizagem Espacial , Animais , Dieta da Carga de Carboidratos/efeitos adversos , Dieta Hiperlipídica/efeitos adversos , Masculino , Estado Pré-Diabético/etiologia , Estado Pré-Diabético/terapia , Ratos , Ratos Sprague-Dawley
17.
Nutrients ; 12(10)2020 Sep 24.
Artigo em Inglês | MEDLINE | ID: mdl-32987812

RESUMO

Diet-induced maternal obesity might play a critical role in altering hypothalamic development, predisposing the offspring to obesity and metabolic disease later in life. The objective of this study was to describe both phenotypic and molecular sex differences in peripubertal offspring energy homeostasis, using a mouse model of maternal obesity induced by a high-fat-high-carbohydrate (HFHC) diet. We report that males, not females, exposed to a maternal HFHC diet had increased energy intake. Males exposed to a maternal HFHC diet had a 15% increased meal size and a 46% increased frequency, compared to the control (CON) males, without a change in energy expenditure. CON and HFHC offspring did not differ in body weight, composition, or plasma metabolic profile. HFHC diet caused decreased hypothalamic glucocorticoid expression, which was further decreased in males compared to females. Maternal weight, maternal caloric intake, and male offspring meal frequency were inversely correlated with offspring hypothalamic insulin receptor (IR) expression. There was a significant interaction between maternal-diet exposure and sex in hypothalamic IR. Based on our preclinical data, we suggest that interventions focusing on normalizing maternal nutrition might be considered to attenuate nutritional influences on obesity programming and curb the continuing rise in obesity rates.


Assuntos
Apetite , Dieta da Carga de Carboidratos/efeitos adversos , Dieta Hiperlipídica/efeitos adversos , Obesidade Materna/sangue , Efeitos Tardios da Exposição Pré-Natal , Hormônio Adrenocorticotrópico/sangue , Animais , Peso Corporal , Colesterol/sangue , Corticosterona/sangue , Metabolismo Energético , Feminino , Hipotálamo/metabolismo , Insulina/sangue , Leptina/sangue , Masculino , Fenômenos Fisiológicos da Nutrição Materna , Camundongos , Camundongos Endogâmicos C57BL , Obesidade Materna/etiologia , Gravidez , Receptor de Insulina/metabolismo , Caracteres Sexuais , Triglicerídeos/sangue
18.
Am J Chin Med ; 48(6): 1409-1433, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32907360

RESUMO

Scutellaria baicalensis (SB), a herbal medicine, is commonly used to treat metabolic diseases, while Metformin (MF) is a widely used drug for type 2 diabetes. The purpose of this study was to investigate whether co-treatment of SB with MF could produce a potential therapeutic effect on high-fat and high-fructose diet (HFFD)-induced metabolic dysregulation. First, we optimized the dose of SB (100, 200, 400, and 800[Formula: see text]mg/kg) with MF (200[Formula: see text]mg/kg) in HFFD-induced C57BL6J mice. Next, the optimized dose of SB (400[Formula: see text]mg/kg) was co-administered with MF (50, 100, and 200[Formula: see text]mg/kg) in a similar animal model to find the effective combinations of SB and MF. Metabolic markers were determined in serum and tissues using different assays, histology, gene expression, and gut microbial population. The SB and MF co-treatment significantly decreased the body, liver, and VAT weights. The outcome of OGTT was improved, and the fasting insulin, HbA1c, TG, TC, LDL-c, AST, and ALT were decreased, while HDL-c was significantly increased. Histological analyses revealed maintained the integrity of liver, adipose tissue, and intestine prevented lipid accumulation in the liver and intestine and combated neuronal damage in the brain. Importantly, controlled the expression of PPAR[Formula: see text], and IL-6 genes in the liver, and expression of BDNF, Glut1, Glut3, and Glut4 genes in the brain. Treatment-specific gut microbial segregation was observed in the PCA chart. Our findings indicate that SB and MF co-treatment is an effective therapeutic approach for HFFD-induced metabolic dysregulation which is operated through the gut-liver-brain axis.


Assuntos
Encéfalo/metabolismo , Microbioma Gastrointestinal , Fígado/metabolismo , Doenças Metabólicas/tratamento farmacológico , Doenças Metabólicas/metabolismo , Metformina/administração & dosagem , Metformina/farmacologia , Fitoterapia , Extratos Vegetais/administração & dosagem , Extratos Vegetais/farmacologia , Animais , Fator Neurotrófico Derivado do Encéfalo/genética , Fator Neurotrófico Derivado do Encéfalo/metabolismo , Dieta da Carga de Carboidratos/efeitos adversos , Dieta Hiperlipídica/efeitos adversos , Modelos Animais de Doenças , Quimioterapia Combinada , Transportador de Glucose Tipo 1/genética , Transportador de Glucose Tipo 1/metabolismo , Interleucina-6/genética , Interleucina-6/metabolismo , Masculino , Doenças Metabólicas/genética , Doenças Metabólicas/microbiologia , Camundongos Endogâmicos C57BL , PPAR gama/genética , PPAR gama/metabolismo
19.
Nutrients ; 12(8)2020 Jul 30.
Artigo em Inglês | MEDLINE | ID: mdl-32751772

RESUMO

While the detrimental effect of refined sugars on health has been the subject of many investigations, little is known about the long-term impact of natural sweeteners on metabolic disorders. In this study we compared the metabolic responses to chronic ingestion of refined sugars compared to various natural sweeteners in diet-induced obese rats. Wistar rats were fed a high-fat high-sucrose diet (HFHS) for 8 weeks and daily gavaged with a solution containing 1 g of total carbohydrates from refined sugar (sucrose or fructose) or six different natural sugar sources, followed by assessment of glucose homeostasis, hepatic lipid accumulation, and inflammation. While glucose tolerance was similar following treatments with refined and natural sugars, lowered glucose-induced hyperinsulinemia was observed with fructose. Consumption of fructose and all-natural sweeteners but not corn syrup were associated with lower insulin resistance as revealed by reduced fasting insulin and homeostatic model assessment of insulin resistance (HOMA-IR) compared to sucrose treatment of HFHS-fed rats. All-natural sweeteners and fructose induced similar liver lipid accumulation as sucrose. Nevertheless, maple syrup, molasses, agave syrup, and corn syrup as well as fructose further reduced hepatic IL-1ß levels compared to sucrose treatment. We conclude that natural sweeteners and especially maple syrup, molasses, and agave syrup attenuate the development of insulin resistance and hepatic inflammation compared to sucrose in diet-induced obese rats, suggesting that consumption of those natural sweeteners is a less harmful alternative to sucrose in the context of obesity.


Assuntos
Dieta da Carga de Carboidratos/efeitos adversos , Fígado Gorduroso/metabolismo , Frutose/farmacologia , Obesidade/metabolismo , Sacarose/farmacologia , Edulcorantes/farmacologia , Animais , Dieta Hiperlipídica/efeitos adversos , Modelos Animais de Doenças , Fígado Gorduroso/etiologia , Resistência à Insulina , Metabolismo dos Lipídeos/efeitos dos fármacos , Fígado/metabolismo , Obesidade/etiologia , Ratos , Ratos Wistar
20.
Int J Mol Sci ; 21(15)2020 Jul 31.
Artigo em Inglês | MEDLINE | ID: mdl-32752013

RESUMO

Gut microbiota-dependent metabolites, in particular trimethylamine (TMA), are linked to hypertension. Maternal 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) exposure or consumption of food high in fructose (HFR) can induce hypertension in adult offspring. We examined whether 3,3-maternal dimethyl-1-butanol (DMB, an inhibitor of TMA formation) therapy can protect adult offspring against hypertension arising from combined HFR and TCDD exposure. Pregnant Sprague-Dawley rats received regular chow or chow supplemented with fructose (60% diet by weight) throughout pregnancy and lactation. Additionally, the pregnant dams received TCDD (200 ng/kg BW orally) or a corn oil vehicle on days 14 and 21 of gestation, and days 7 and 14 after birth. Some mother rats received 1% DMB in their drinking water throughout pregnancy and lactation. Six groups of male offspring were studied (n = 8 for each group): regular chow (CV), high-fructose diet (HFR), regular diet+TCDD exposure (CT), HFR+TCDD exposure (HRT), high-fructose diet+DMB treatment (HRD), and HFR+TCDD+DMB treatment (HRTD). Our data showed that TCDD exacerbates HFR-induced elevation of blood pressure in male adult offspring, which was prevented by maternal DMB administration. We observed that different maternal insults induced distinct enterotypes in adult offspring. The beneficial effects of DMB are related to alterations of gut microbiota, the increase in nitric oxide (NO) bioavailability, the balance of the renin-angiotensin system, and antagonization of aryl hydrocarbon receptor (AHR) signaling. Our findings cast new light on the role of early intervention targeting of the gut microbiota-dependent metabolite TMA, which may allow us to prevent the development of hypertension programmed by maternal excessive fructose intake and environmental dioxin exposure.


Assuntos
Dieta da Carga de Carboidratos/efeitos adversos , Microbioma Gastrointestinal , Hipertensão , Exposição Materna/efeitos adversos , Efeitos Tardios da Exposição Pré-Natal , Animais , Dioxinas/efeitos adversos , Feminino , Frutose/efeitos adversos , Masculino , Metilaminas/farmacologia , Gravidez , Substâncias Protetoras/farmacologia , Ratos , Ratos Sprague-Dawley
SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA
...