Dataset Information

Effects of High-Fat Diet Induced Obesity and Fructooligosaccharide Supplementation on Cardiac Protein Expression.

ABSTRACT: The mechanism by which high fat-diet induced obesity affects cardiac protein expression is unclear, and the extent to which this is modulated by prebiotic treatment is not known. These outcomes were assessed in rats initially fed a high-fat diet, then the top 40% weight gain group were randomly allocated to control (CON), high-fat (HF) and HF supplemented with fructooligosaccharide (32 g; HF-FOS) treatments for 12 weeks (n = 10/group). At sacrifice, left ventricles were either frozen or preserved in formalin. Serum was stored for glucose and insulin measurements. Protein spectra was obtained using an Orbitrap analyzer, processed with Sequest and fold changes assessed with Scaffold Q +. Treatment effects for body weights, glucose and insulin were assessed using one-way ANOVA, and the differential protein expression was assessed by a Mann-Whitney U test. The Database for Annotation, Visualization and Integrated Discovery and the Kyoto Encyclopedia of Genes and Genomes identified pathways containing overrepresented proteins. Hematoxylin and eosin sections were graded for hypertrophy and also quantified; differences were identified using Chi-square analyses and Mann-Whitney U tests. HF diet fed rats were significantly (p < 0.05) heavier than CON, and 23 proteins involved in mitochondrial function and lipid metabolism were differentially expressed between HF and CON. Between HF-FOS and HF, 117 proteins involved in contractility, lipid and carbohydrate metabolism were differentially expressed. HF cardiomyocytes were significantly (p < 0.05) more hypertrophic than CON. We conclude that high-fat feeding and FOS are associated with subcellular deviations in cardiac metabolism and contractility, which may influence myocardial function and alter the risk of cardiovascular disease.

SUBMITTER: Sarfaraz S

PROVIDER: S-EPMC7694524 | biostudies-literature | 2020 Nov

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Effects of High-Fat Diet Induced Obesity and Fructooligosaccharide Supplementation on Cardiac Protein Expression.

Sarfaraz Sidra S Singh Shamjeet S Hawke Aileen A Clarke Sandra T ST Ramdath D Dan DD

Nutrients 20201105 11

The mechanism by which high fat-diet induced obesity affects cardiac protein expression is unclear, and the extent to which this is modulated by prebiotic treatment is not known. These outcomes were assessed in rats initially fed a high-fat diet, then the top 40% weight gain group were randomly allocated to control (CON), high-fat (HF) and HF supplemented with fructooligosaccharide (32 g; HF-FOS) treatments for 12 weeks (<i>n</i> = 10/group). At sacrifice, left ventricles were either frozen or p ...[more]

PMID: 33167590

Similar Datasets

Project description:Reduced hepatic glycogenesis is one of the most important causes of metabolic abnormalities in non‑alcoholic fatty liver disease. Octreotide, a somatostatin analogue, has been demonstrated to promote weight loss and improve metabolic disorders in mice with high fat diet (HFD)‑induced obesity. However, whether octreotide affects hepatic glycogenesis is unknown. The aim of the present study was to verify the effects of octreotide on hepatic glycogenesis in rats with HFD‑induced obesity. Male Sprague‑Dawley rats were fed a standard diet or a HFD for 24 weeks. Obese rats from the HFD group were further divided into a HFD‑control group and an octreotide‑administered group. Rats in the latter group were injected with octreotide for 8 days. Glucose and insulin tolerance tests were performed, and the area under the curve (AUC) was calculated. Following sacrifice, their body weights and lengths, fasting plasma glucose (FPG), fasting insulin (FINS), serum triglyceride (TG), total cholesterol (TC), free fatty acid (FFA), alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels were measured. In addition, Lee's index and the homeostatic model assessment index were calculated. Hepatic TG, FFA levels and glycogen content were first determined. Hepatic steatosis in the obese rats was assessed based on hematoxylin and eosin and Oil Red O staining. Human hepatoblastoma HepG2 cells were divided into a control group, a palmitate (PA)‑treated group and a PA + octreotide‑treated group. Establishment of the in vitro fatty liver model using HepG2 cells was confirmed by Oil Red O staining. The expression of phosphorylated Akt and glycogen synthase kinase 3β (GSK3β) was detected by western blotting, and glycogen synthase (GS) mRNA levels were detected by reverse transcription‑quantitative polymerase chain reaction. Compared with the control group, the body weight, Lee's index, AUC of the intraperitoneal glucose tolerance test and intraperitoneal insulin tolerance test, levels of FPG, FINS, TG, TC, FFA, ALT and AST, and HOMA index values were significantly increased in the obese rats. The body weight, levels of FPG and FINS, and the HOMA index were significantly reduced following octreotide treatment, whereas the decrease in Lee's index, the blood levels of ALT, AST, TC, TG and FFA, and the AUC did not reach statistical significance. Hepatic TG and FFA levels were significantly increased and hepatic glycogen content was significantly decreased in rats with HFD‑induced obesity when compared with those in the control group. Octreotide intervention restored these alterations. The expression levels of phosphorylated Akt and GSK3β protein expression, as well as GS mRNA levels in the HFD group were lower when compared with those in the control group, whereas octreotide treatment reversed these reductions. The in vitro experiments demonstrated that the reduced levels of phosphorylated Akt and GSK3β protein, and GS mRNA in the PA‑treated group were significantly reversed by octreotide treatment. In conclusion, the results indicate that octreotide improved hepatic glycogenesis and decreased FPG concentration in rats with HFD‑induced obesity. These mechanisms may be associated with increased GS activity via the promotion of GSK3β phosphorylation. Therefore, octreotide may be regarded as a novel therapeutic strategy for HFD‑induced obesity and obesity‑associated metabolic disorders.

Dataset Information

Effects of High-Fat Diet Induced Obesity and Fructooligosaccharide Supplementation on Cardiac Protein Expression.

Publications

Effects of High-Fat Diet Induced Obesity and Fructooligosaccharide Supplementation on Cardiac Protein Expression.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets