Chronic Intake of High-Fat and High-Sucrose Diets Differentially Affects Glucose Intolerance in Mice

Abstract

Intakes of some macronutrients can comprise risk factors for life-style-related diseases such as obesity, hyperlipidemia, diabetes, hypertension, and atherosclerosis. In this study, we examined the effects in C57BL/6J mice of consuming excess fat or sucrose for a long period of time (55 wk). Another group of mice consumed a low-fat, low-sucrose (LL) diet. Mice fed the high-fat (HF) diet gained weight and developed hyperlipidemia and hyperleptinemia. At 25 wk, but not at 55 wk, hepatic glucose-6-phosphatase (G6Pase) activity of the mice fed the high sucrose (HS) diet was greater than that of mice fed the LL or HF diet. Those fed the HS diet were not obese and had greater hepatic lipogenic and gluconeogenic enzyme activities. The HF and HS diets resulted in different types of glucose intolerance. In an oral glucose tolerance test, mice fed the HF diet had a delay in the clearance of glucose compared with those fed the LL diet, perhaps due to the peripheral insulin resistance that resulted from higher levels of circulating free fatty acids. Feeding the HS diet for 55 wk induced hyperglycemia 10 min after oral glucose administration, although blood glucose declined rapidly after i.p. insulin injection. This finding suggests that the effects of chronic HS diet intake may be due to the reduction in early insulin secretion from pancreatic islets and the increase in sucrase activity in the small intestine. It is important to consider the effects of macronutrients in lean as well as obese mice to clarify the pathogenesis of the metabolic disorders.

Early and Long-term Undernutrition in Female Rats Exacerbates the Metabolic Risk Associated with Nutritional Rehabilitation

“…Increased brite adipocyte levels and hyperexpression of ectopic UCP-1 confer resistance to diet-induced obesity (42,43), as probably occurs in the undernourished rats. Dyslipidemia, Ectopic Lipids, and Oxidative Stress-The cafeteria formula did not modify either triglyceridemia or cholesterolemia in the control rats, in contrast to other regimes richer in fat (44). When the undernourished were transferred to lab chow, their reduced triglyceride levels persisted.…”

Metabolic disturbances induce malignant heart arrhythmias in rats

“…Commonly used rat models are spontaneous hypertensive rats and Sprague Dawley rats, both strains fed with high-sugar diet (33). Although high-fat diet models and high-sucrose models have different effects on the metabolism, both facilitate metabolic disorders (34). Spontaneous HTG rats and HTG rats fed high-fat diet both resemble signs of the metabolic syndrome (31).…”

Animal Models of Nutritional Induction of Type 2 Diabetes Mellitus

“…Solid food with a normal fat content failed to induce obesity and hyperinsulinemia in C57BL/6J mice (Sumiyoshi et al, 2006). However, a recent study demonstrated that although a sucrose-rich diet (32%) does not lead to obesity in C57BL/6 mice, the diet has the potential to cause changes in adipocytes (hypertrophy), as well as glucose intolerance, hyperinsulinemia, hyperlipidemia, hepatic steatosis and increased levels of inflammatory cytokines (Oliveira et al, 2014).…”