Consuming decaffeinated coffee with milk and sugar added before a high-glycaemic index meal improves postprandial glycaemic and insulinaemic responses in healthy adults.

The present study aimed to compare the effects of drinking different types of coffee before a high-glycaemic index (GI) meal on postprandial glucose metabolism and to assess the effects of adding milk and sugar into coffee. In this randomised, crossover, acute feeding study, apparently healthy adults (n 21) consumed the test drink followed by a high-GI meal in each session. Different types of coffee (espresso, instant, boiled and decaffeinated, all with milk and sugar) and plain water were tested in separate sessions, while a subset of the participants (n 10) completed extra sessions using black coffees. Postprandial levels of glucose, insulin, active glucagon-like peptide 1 (GLP-1) and nitrotyrosine between different test drinks were compared using linear mixed models. Results showed that only preloading decaffeinated coffee with milk and sugar led to significantly lower glucose incremental AUC (iAUC; 14 % lower, P = 0·001) than water. Preloading black coffees led to greater postprandial glucose iAUC than preloading coffees with milk and sugar added (12-35 % smaller, P < 0·05 for all coffee types). Active GLP-1 and nitrotyrosine levels were not significantly different between test drinks. To conclude, preloading decaffeinated coffee with milk and sugar led to a blunted postprandial glycaemic response after a subsequent high-GI meal, while adding milk and sugar into coffee could mitigate the impairment effect of black coffee towards postprandial glucose responses. These findings may partly explain the positive effects of coffee consumption on glucose metabolism.

Maternal green tea extract supplementation to rats fed a high-fat diet ameliorates insulin resistance in adult male offspring.

Maternal overnutrition is associated with increased risk of metabolic disorders in the offspring. This study tested the hypothesis that maternal green tea (GT) supplementation can alleviate metabolic derangements in high-fat-diet-fed rats born of obese dams. Female Sprague-Dawley rats were fed low-fat (LF, 7%), high-fat (HF, 30%) or HF diet containing 0.75% or 1.0% GT extract (GT1, GT2) prior to conception and throughout gestation and lactation. Both doses of GT significantly improved metabolic parameters of HF-fed lactating dams (P<.05). Birth weight and litter size of offspring from HF dams were similar, but GT supplementation led to lighter pups on day 21 (P<.05). The weaned male pups received HF, GT1 or GT2 diet (dam/pup diet groups: LF/HF, HF/HF, HF/GT1, HF/GT2, GT1/HF and GT2/HF). At week 13, they had similar weight but insulin resistance index (IRI), serum nonesterified fatty acid (NEFA) and liver triglyceride of rats born to GT dams were 57%, 23% and 26% lower, accompanied by improved gene/protein expressions related to lipid and glucose metabolism, compared with the HF/HF rats (P<.05). Although HF/GT1 and HF/GT2 rats had lower serum NEFA, their insulin and IRI were comparable to HF/HF rats. This study shows that metabolic derangements induced by an overnourished mother could be offset by supplementing GT to the maternal diet and that this approach is more effective than giving GT to offspring since weaning. Hence, adverse effects of developmental programming are reversible, at least in part, by supplementing bioactive food component(s) to the mother's diet.

Supplementation of bitter melon to rats fed a high-fructose diet during gestation and lactation ameliorates fructose-induced dyslipidemia and hepatic oxidative stress in male offspring.

This study examined the impact of maternal high-fructose intake and if metabolic control in the offspring could benefit from supplementing bioactive food components such as bitter melon (BM) to the maternal diet. In Expt. 1, virgin female rats received control (C), high-fructose (F; 60%), or BM-supplemented fructose (FBM; 1%) diet before conception until d 21 of lactation. Weaned male offspring were fed the C diet for 11 wk, forming C/C, F/C, and FBM/C groups. The F/C group had elevated serum insulin, TG, and FFA concentrations and hepatic lipid alterations compared with the C/C and FBM/C groups (P < 0.05). The 2 latter groups did not differ. Expt. 2 had similar dam treatment groups, but offspring were weaned to the C or F diet, forming C/C, C/F, F/F, and FBM/F groups, and the dietary treatment was extended to 20 wk. The hepatic levels of stearyl-CoA desaturase and microsomal TG transfer protein mRNA were lower, but that of PPARγ coactivator 1-α and fibroblast growth factor 21 mRNA and fatty acid binding protein 1 protein were higher in the FBM/F group compared with the C/F and F/F groups (P < 0.05), indicating that maternal BM supplementation may reduce lipogenesis and promote lipid oxidation in offspring. The FBM/F group had significantly higher activities of liver glutathione peroxidase, superoxide dismutase, and catalase than the F/F group. The results indicate that supplementing BM to dams could offset the adverse effects of maternal high-fructose intake on lipid metabolism and antioxidant status in adult offspring.

Dietary fat concentration influences the effects of trans-10, cis-12 conjugated linoleic acid on temporal patterns of energy intake and hypothalamic expression of appetite-controlling genes in mice.

This study tested the hypothesis that the effect of trans-10, cis-12 conjugated linoleic acid (t10, c12 CLA) on energy intake (EI) and body weight (BW)/composition is confounded by dietary fat concentration and involves hypothalamic appetite-controlling mechanisms. ICR mice received low-fat (LF; 5 g/100 g) or high-fat (HF; 30 g/100 g) diets, with or without 0.5 g/100 g t10, c12 CLA (>98% pure) for 27 d. By d 13, BW and cumulative EI of the mice fed CLA supplemented LF diet (LF/CLA) were 6.6 and 23.6% lower, respectively, than the LF mice. In the subsequent 14 d, their EI rebounded and did not differ from the LF group. BW and EI did not differ between the HF and CLA supplemented HF (HF/CLA) groups. Hypothalamic pro-opiomelanocortin (POMC) mRNA expression was elevated (P = 0.031) on d 13 but suppressed (P < 0.001) on d 27 due to CLA treatment. CLA also suppressed AMP-activated protein kinase alpha2 expression. Mice in Expt. 2 received the LF diet, the LF/CLA, or were pair-fed the LF diet to the EI of the CLA group (LF/PF). LF/CLA and LF/PF mice did not differ in the hypothalamic POMC:neuropeptide Y expression ratio on d 13, but it was significantly lower in the LF/PF group on d 27. We conclude that the habitual dietary fat concentration influences the magnitude of weight loss induced by dietary t10, c12 CLA. The effect is in part independent of EI. Hypothalamic neuropeptides and nutrient sensing mechanisms may play a role.