This study evaluated the effects and the underlying mechanisms of casein glycomacropeptide hydrolysate (GHP) on high-fat diet-fed and streptozotocin-induced type 2 diabetes (T2D) in C57BL/6J mice. Results showed that 8-week GHP supplementation significantly decreased fasting blood glucose levels, restored insulin production, improved glucose tolerance and insulin tolerance, and alleviated dyslipidemia in T2D mice. In addition, GHP supplementation reduced the concentration of lipopolysaccharides (LPSs) and pro-inflammatory cytokines in serum, which led to reduced systematic inflammation. Furthermore, GHP supplementation increased muscle glycogen content in diabetic mice, which was probably due to the regulation of glycogen synthase kinase 3 beta and glycogen synthase. GHP regulated the insulin receptor substrate-1/phosphatidylinositol 3-kinase/protein kinase B pathway in skeletal muscle, which promoted glucose transporter 4 (GLUT4) translocation. Moreover, GHP modulated the overall structure and diversity of gut microbiota in T2D mice. GHP increased the Bacteroidetes/Firmicutes ratio and the abundance of S24-7, Ruminiclostridium, Blautia and Allobaculum, which might contribute to its antidiabetic effect. Taken together, our findings demonstrate that the antidiabetic effect of GHP may be associated with the recovery of skeletal muscle insulin sensitivity and the regulation of gut microbiota.

Promoting brown adipose tissue (BAT) function or browning of white adipose tissue (WAT) provides a defense against obesity. The aim of the study was to investigate whether maternal polar lipids‐enriched milk fat globule membrane (MFGM‐PL) supplementation to high‐fat diet (HFD) rats during pregnancy and lactation could promote brown/beige adipogenesis and protect against HFD‐induced adiposity in offspring. Female SD rats were fed a HFD for 8 weeks to induce obesity and, then, fed a HFD during pregnancy and lactation with or without MFGM‐PL. Male offspring were weaned at postnatal Day 21 and then fed a HFD for 9 weeks. MFGM‐PL treatment to HFD dams decreased the body weight gain and WAT mass as well as lowered the serum levels of insulin and triglycerides in male offspring at weaning. MFGM‐PL+HFD offspring showed promoted thermogenic function in BAT and inguinal WAT through the upregulation of UCP1 and other thermogenic genes. In adulthood, maternal MFGM‐PL supplementation reduced adiposity and increased oxygen consumption, respiratory exchange ratio, and heat production in male offspring. The enhancement of energy expenditure was correlated with elevated BAT activity and inguinal WAT thermogenic program. In conclusion, maternal MFGM‐PL treatment activated thermogenesis in offspring, which exerted long‐term beneficial effects against HFD‐induced obesity in later life.

Scope: Milk fat globule membrane (MFGM), which contains abundant polar lipids and glycoproteins, can narrow the gap in growth and development between breast-fed and infant-formula-fed babies. The objective of this study is to evaluate the effect of MFGM supplementation in infant formula on intestinal epithelium maturation, tight junctions, and gut colonization in rat pups. Methods and results: Sprague Dawley rat pups consume one of the five diets from postnatal day 8, including rat breastfeeding (BF), infant formula (IF), and infant formula containing MFGM at 260 mg kg −1 body weight (BW), 520 mg kg −1 BW, or 1040 mg kg −1 BW. Results show that MFGM supplementation in infant formula can facilitate intestinal mucosal barrier maturation via promoting intestinal proliferation and differentiation, and increasing tight junction proteins. In addition, compared with that of the IF pups, the intestinal flora composition of MFGM-supplemented pups is more similar to that of BF pups. Conclusion: MFGM supplementation in infant formula can restore the intestinal development in infant-formula-fed pups, which suggests that the supplementation of MFGM in infant formula can better mimic breast milk.

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