Abstract
BackgroundDiets producing a high glycemic response result in exaggerated insulin secretion which induces hepatic lipogenesis, contributing to development of insulin resistance and fatty liver. Viscous dietary fibers blunt the postprandial rise in blood glucose, however their effect on type 2 diabetes and obesity are not entirely known. This study examined the effect of chronic consumption of the viscous, non-fermentable dietary fiber, hydroxypropyl methylcellulose (HPMC), on glucose control, insulin resistance and liver lipids in an obese diabetic rat model.MethodsThree groups of Zucker Diabetic Fatty (ZDF) rats were fed diets containing either 5% non-viscous cellulose (control), low viscosity HPMC (LV-HPMC) or high viscosity HPMC (HV- HPMC) for six weeks. Zucker lean littermates consuming cellulose served as a negative control. Markers of glucose control, including oral glucose tolerance test, glycated hemoglobin and urinary glucose, were measured as well as adiposity and the accumulation of liver lipids.ResultsThe HPMC diets increased the viscosity of the small intestinal contents and reduced the postprandial rise in blood glucose. The food efficiency ratio was greater with HPMC feeding compared to the obese control and urinary excretion of glucose and ketone bodies was reduced. The two HPMC groups had lower glycated hemoglobin and kidney weights and a reduced area under the curve during a glucose tolerance test, indicating improved glucose control. Epididymal fat pad weight as percent of body weight was reduced in the HV-HPMC group compared to the obese control group. The HV-HPMC group also had lower concentrations of liver lipid and cholesterol and reduced liver weight. However, HV-HPMC feeding did not affect hepatic gene expression of SREBP-1c or FAS. Muscle concentration of acylcarnitines, a lipid intermediate in fatty acid β-oxidation, was not different between the HPMC groups and obese control, suggesting no change in muscle fatty acid oxidation by HPMC.ConclusionsConsumption of the viscous non-fermentable fiber HPMC decreased diabetic wasting, improved glucose control and reduced insulin resistance and fatty liver in a model of obesity with diabetes.
Highlights
Diets producing a high glycemic response result in exaggerated insulin secretion which induces hepatic lipogenesis, contributing to development of insulin resistance and fatty liver
The Total area under the curve (tAUC) of the postprandial glucose curve after a meal (Table 1) in the LV-hydroxypropyl methylcellulose (HPMC) and High viscosity HPMC (HVHPMC) groups was significantly less than the obese control, and the tAUC of the high viscosity HPMC (HV-HPMC) did not differ significantly from the lean control group
Our results show increased short and long chain acylcarnitines in the three Zucker Diabetic Fatty (ZDF) groups compared to the lean control but, surprisingly, the HV-HPMC group, which displayed less insulin resistance compared to the obese control group, as shown by an improved Oral glucose tolerance tests (OGTT) and a higher quantitative insulin sensitivity check index (QUICKI), did not differ from the obese control in acylcarnitine concentration in the muscle
Summary
Diets producing a high glycemic response result in exaggerated insulin secretion which induces hepatic lipogenesis, contributing to development of insulin resistance and fatty liver. Viscous dietary fibers blunt the postprandial rise in blood glucose, their effect on type 2 diabetes and obesity are not entirely known. This study examined the effect of chronic consumption of the viscous, non-fermentable dietary fiber, hydroxypropyl methylcellulose (HPMC), on glucose control, insulin resistance and liver lipids in an obese diabetic rat model. Hyperglycemia, resulting from rapidly absorbed glucose from a meal, will greatly stimulate insulin secretion, causing a large increase in plasma insulin. This exaggerated insulin response to a meal will alter the normal homeostatic control of plasma glucose and non-esterified fatty acids and increase glycogenesis and lipogenesis in the liver as well as increase glucose uptake by insulin-sensitive tissues. A slower absorption of glucose was found to decrease the insulin response and decrease hepatic lipogenic gene expression [7]
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