Abstract

BackgroundConsumption of dairy products reduces risk of type 2 diabetes. Milk proteins and fats exhibit anti-diabetic properties but milk sugars have been studied little in this context. Galactose from milk lactose is readily converted to glycogen in the liver but its effects on insulin sensitivity have not been assessed. Prebiotic oligosaccharides from milk alter gut microbiota and can thereby influence host metabolism. Our objective was to assess the effect on insulin sensitivity of dietary galactose compared to glucose and fructose, and fermentable galacto-oligosaccharides compared to non-fermentable methylcellulose.MethodsDiets containing 15% of dry matter from glucose, fructose, galactose, galacto-oligosaccharides, or methylcellulose were fed to 36 rats per diet for 9 weeks. Hyperinsulinemic-euglycemic clamps with [3-3H]glucose infusion and a steady-state 2-[1-14C]deoxyglucose bolus injection were used to assess insulin sensitivity and glucose uptake indices. Tissue was collected in fed, fasted and fasted, insulin-stimulated states.ResultsGalactose increased glucose infusion rate during the clamp by 53% and decreased endogenous glucose production by 57% compared to glucose and fructose. Fed-state hepatic glycogen content was greater with galactose compared to glucose and fructose, consistent with a potentiation of the insulin effect on glycogen synthase by dephosphorylation. Galactose decreased the fecal Firmicutes:Bacteroidetes ratio while galacto-oligosaccharides increased abundance of fecal Bifidobacterium spp. 481-fold compared to methylcellulose, and also increased abundance of Lactobacillus spp. and Bacteroidetes. Galacto-oligosaccharides did not affect glucose infusion rate or endogenous glucose production during basal or clamp periods compared to methylcellulose.ConclusionsGalactose at 15% of daily intake improved hepatic insulin sensitivity in rats compared to glucose and fructose. Galactose caused an increase in fed-state hepatic glycogen content and a favourable shift in gut microbial populations. Intake of galacto-oligosaccharides improved the gut microbial profile but did not improve insulin sensitivity.

Highlights

  • Epidemiological studies assessing dairy product consumption by questionnaire [1,2] and biomarker analyses [3] have linked increased dairy consumption with decreased markers of metabolic syndrome

  • Our objective was to assess the effect on insulin sensitivity of dietary galactose compared to glucose and fructose, and fermentable galactooligosaccharides compared to non-fermentable methylcellulose

  • Fed-state hepatic glycogen content was greater with galactose compared to glucose and fructose, consistent with a potentiation of the insulin effect on glycogen synthase by dephosphorylation

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Summary

Introduction

Epidemiological studies assessing dairy product consumption by questionnaire [1,2] and biomarker analyses [3] have linked increased dairy consumption with decreased markers of metabolic syndrome. The milk sugars, lactose and galacto-oligosaccharides, have been studied little in the context of insulin sensitivity, there is reason to expect positive effects. Lactose contains the simple sugar galactose which, unlike the glucose and fructose moieties of sucrose, passes completely into hepatic glycogen upon absorption [12]. This glycogenic effect may impact whole-body glucose utilization and insulin sensitivity, such effects have not yet been studied, to our knowledge. [16] These favourable shifts in gut microbiota may improve hepatic metabolism and insulin sensitivity in the host by altering colonic short-chain fatty acid production, gut peptide secretion and gut barrier function [17]. Our objective was to assess the effect on insulin sensitivity of dietary galactose compared to glucose and fructose, and fermentable galactooligosaccharides compared to non-fermentable methylcellulose

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