Diet high in fat and sucrose induces rapid onset of obesity-related metabolic syndrome partly through rapid response of genes involved in lipogenesis, insulin signalling and inflammation in mice

Abstract

BackgroundFrequent consumption of a diet high in fat and sucrose contributes to lifestyle-related diseases. However, limited information is available regarding the short-term effects of such a diet on the onset of obesity-associated metabolic abnormalities.MethodsMale C57BL/6 J mice were divided into two groups and fed a standard chow diet (control group) or a high fat–high sucrose diet containing 21% fat and 34% sucrose (HF–HS diet group) for 2 or 4 weeks.ResultsThe HF–HS diet significantly induced body weight gain beginning at week 1 and similarly increased mesenteric white adipose tissue weight and plasma insulin levels at weeks 2 and 4. Plasma resistin levels were notably elevated after feeding with the HF–HS diet for 4 weeks. Measurement of hepatic triglycerides and Oil Red O staining clearly indicated increased hepatic lipid accumulation in response to the HF–HS diet as early as 2 weeks. Quantitative PCR analysis of liver and white adipose tissue indicated that, starting at week 2, the HF–HS diet upregulated mRNA expression from genes involved in lipid metabolism and inflammation and downregulated genes involved in insulin signalling. Although plasma cholesterol levels were also rapidly increased by the HF–HS diet, no differences were found between the control and HF–HS diet–fed animals in the expression of key genes involved in cholesterol biosynthesis.ConclusionsOur study demonstrates that the rapid onset of hepatosteatosis, adipose tissue hypertrophy and hyperinsulinemia by ingestion of a diet high in fat and sucrose may possibly be due to the rapid response of lipogenic, insulin signalling and inflammatory genes.

Anti-obesity effects of Taif and Egyptian pomegranates: molecular study

“…The downregulation of PK in obesity group and its upregulation after pomegranate juice treatment corresponds to insulin level in both conditions, as insulin was reported to upregulate PK in rat hepatocytes. 57) Parallel to molecular findings and in agreement with previous studies, 39,58,59) histological examination revealed fatty degeneration of hepatocytes (steatosis) in hepatic sections stained by oil red O from rats in groups received HFD, but not in the control group. Hepatic sections from rats in groups received HFD concurrently with pomegranate juices revealed remarkable reduction in the size and number of lipid droplets.…”

Restriction on an Energy-Dense Diet Improves Markers of Metabolic Health and Cellular Aging in Mice Through Decreasing Hepatic mTOR Activity

“…The HFDR ameliorated metabolic dysfunction and mitigated hyperactivation of growth factor-related signaling, such as mTOR and insulin. Our data indicate that a simple reduction of the absolute intake of an otherwise adverse diet 23 may improve metabolic health and impede cellular aging, e.g. through induction of chaperone-mediated autophagy.…”

“…The experimental diet was a purified semi-synthetic, energy-dense, high-fat, and high-sugar diet purchased from Ssniff (TD 88137 modified; Soest, Germany) that is known to rapidly induce body weight gain and adipose tissue hypertrophy in C57BL/6 mice. 23 The diet contained 17.1 grams/kg crude protein, 21.2 grams/kg crude fat, 14.5 grams/kg starch, and 32.8 grams/kg sucrose. The metabolizable energy of the diet (19.1 MJ/kg) was composed of 43% carbohydrates, 15% protein, and 42% fat with a protein-to-carbohydrate ratio of 0.35.…”

Green Tea Polyphenol Epigallocatechin-3-gallate Suppresses Toll-like Receptor 4 Expression via Up-regulation of E3 Ubiquitin-protein Ligase RNF216

“…Recent studies suggest that chronic low-grade inflammation is a characteristic of obesity (31,32). Moreover, macrophage activation in the adipose tissue is a crucial step that drives the development of obesity and related diseases (32).…”