12 pubs · 467 cites · h-index 5
Introduction: T63 has been shown to improve fasting blood glucose (FG) in individuals with prediabetes or early type 2 diabetes. However, the mechanisms underlying these effects are still unknown. We sought to assess the effects of T63 on fasting and postprandial (PP) metabolic parameters as well as on the gut microbiota. Methods: In this 8-wk, single arm, open label, clinical trial (NCT05369585), a daily dose of 5g of T63 was given by capsules. Eligible participants had a BMI ≥27 and <40kg/m2, and either triglycerides (TG) ≥1.35mmol/L, or FG ≥5.6 and ≤6.9mmol/L, or HbA1c ≥5.6 and ≤6.4%. Blood was sampled fasting and during a 6-hour test meal for analysis of glucose homeostasis, lipids, hs-CRP, fibrinogen and incretins. Assessments were made before and after an acute intake as well as after 8 wk of supplementation. The fecal microbiota was analysed by metagenomic sequencing and the Simpson’s reciprocal index used for determination of microbial diversity. Results: A total of 19 participants were enrolled and supplemented, (mean±SD) age 55.4±11.3 yrs, BMI 31.3±4.1kg/m2, FG 5.5±0.4mmol/L, HbA1c 5.5±0.2%, TG 1.6±0.5mmol/L, hs-CRP 3.3±2.3mg/L. Following the first acute T63 intake, PP reductions in max glucose level (p=0.03), and GIP area under the curve (AUC, p=0.01) were observed. After 8 wk of T63, significant decreases in HbA1c (to 5.3±0.3%, p=0.005), hs-CRP (to 2.5±1.8mg/L, p=0.01), fibrinogen (p=0.04) and plasma lipids (TG, total-C, non-HDL-C, LDL-C and total-C/HDL-C ratio (p<0.05 for all)) were observed, while PYY increased (p=0.02). The PP pattern at wk 8 was characterized by reductions in the AUC of both glucose (p=0.04) and insulin (p=0.009). Gut microbiota α-diversity was increased by T63 at wk 8 (p=0.003). Conclusion: These results provide novel insights on the effects of T63 on fasting and PP glucose metabolism, inflammation and lipids, in conjunction with an increased gut microbiota diversity. Disclosure A. Bouchard-Mercier: Employee; Valbiotis. Y.F. Otero: Employee; Valbiotis. V. Chavanelle: Employee; Valbiotis. J. Marois: None. G. Pilon: None. T. Varin: None. P.L. Mitchell: None. O. Johansen: Employee; Nestlé Health Science. M. Bargetto: Employee; Valbiotis. V. Sapone: None. F. Le Joubioux: Employee; Valbiotis. M. Cazaubiel: Employee; Valbiotis. J. Bard: Consultant; Valbiotis. Stock/Shareholder; Valbiotis. S. Peltier: Stock/Shareholder; Valbiotis. Board Member; Valbiotis. P. Couture: None. M. Vohl: None. P. Sirvent: Board Member; Valbiotis. A. Marette: Advisory Panel; Valbiotis. Research Support; Acasti Pharma, Inc. Advisory Panel; Plexus, Amancia.
Using an oral glucose tolerance test, we found hyperinsulinemia, lower insulin sensitivity, lower insulin clearance, and lower first-phase pancreatic β-cell function in individuals with MAFLD. This may explain part of the increased risk of incident type 2 diabetes in this population. These data also highlight implications of hyperinsulinemia and impaired insulin clearance in the progression of MAFLD to type 2 diabetes.
The objective of the present study was to test whether a brown seaweed extract rich in polyphenols combined with a low-calorie diet would induce additional weight loss and improve blood glucose homeostasis in association with a metabolic and inflammatory response in overweight/obese prediabetic subjects. Fifty-six overweight/obese, dysglycemic, and insulin-resistant men and women completed a randomized, placebo-controlled, double-blind, and parallel clinical trial. Subjects were administrated 500 mg/d of either brown seaweed extract or placebo combined with individualized nutritional advice for moderate weight loss over a period of 12 weeks. Glycemic, anthropometric, blood pressure, heart rate, body composition, lipid profile, gut integrity, and oxidative and inflammatory markers were measured before and at the end of the trial. No effect was observed on blood glucose. We observed significant but small decreases in plasma C-peptide at 120 min during 2 h-OGTT (3218 ± 181 at pre-intervention vs. 2865 ± 186 pmol/L at post-intervention in the brown seaweed group; 3004 ± 199 at pre-intervention vs. 2954 ± 179 pmol/L at post-intervention in the placebo group; changes between the two groups, p = 0.002), heart rate (72 ± 10 at pre-intervention vs. 69 ± 9 (n/min) at post-intervention in the brown seaweed group; 68 ± 9 at pre-intervention vs. 68 ± 8 (n/min) at post-intervention in the placebo group; changes between the two groups, p = 0.01), and an inhibition in the increase of pro-inflammatory interleukin-6 (IL-6) (1.3 ± 0.7 at pre-intervention vs. 1.5 ± 0.7 pg/L at post-intervention in the brown seaweed group; 1.4 ± 1.1 at pre-intervention vs. 2.2 ± 1.6 pg/L at post-intervention in the placebo group; changes between the two groups, p = 0.02) following brown seaweed consumption compared with placebo in the context of moderate weight loss. Although consumption of brown seaweed extract had no effect on body weight or blood glucose, an early attenuation of the inflammatory response was observed in association with marginal changes in metabolic parameters related to the prevention of diabetes type 2.
Plant-derived foods rich in polyphenols are associated with several cardiometabolic health benefits, such as reduced postprandial hyperglycaemia. However, their impact on whole-body insulin sensitivity using the hyperinsulinaemic-euglycaemic clamp technique remains under-studied. We aimed to determine the effects of strawberry and cranberry polyphenols (SCP) on insulin sensitivity, glucose tolerance, insulin secretion, lipid profile, inflammation and oxidative stress markers in free-living insulin-resistant overweight or obese human subjects (n 41) in a parallel, double-blind, controlled and randomised clinical trial. The experimental group consumed an SCP beverage (333 mg SCP) daily for 6 weeks, whereas the Control group received a flavour-matched Control beverage that contained 0 mg SCP. At the beginning and at the end of the experimental period, insulin sensitivity was assessed by a hyperinsulinaemic-euglycaemic clamp, and glucose tolerance and insulin secretion by a 2-h oral glucose tolerance test (OGTT). Insulin sensitivity increased in the SCP group as compared with the Control group (+0·9 (sem 0·5)×10-3 v. -0·5 (sem 0·5)×10-3 mg/kg per min per pmol, respectively, P=0·03). Compared with the Control group, the SCP group had a lower first-phase insulin secretion response as measured by C-peptide levels during the first 30 min of the OGTT (P=0·002). No differences were detected between the two groups for lipids and markers of inflammation and oxidative stress. A 6-week dietary intervention with 333 mg of polyphenols from strawberries and cranberries improved insulin sensitivity in overweight and obese non-diabetic, insulin-resistant human subjects but was not effective in improving other cardiometabolic risk factors.
Previous studies have shown that fish protein, as well as marine n-3 PUFA, may have beneficial effects on cardiovascular risk profile. The objectives of this study were to investigate the combined effects of fish gelatine (FG) and n-3 PUFA supplementation on (1) energy intake and body weight, (2) lipid profile and (3) inflammatory and CVD markers in free-living insulin-resistant males and females. Subjects were asked to consume, in a crossover study design with two experimental periods of 8 weeks each, an n-3 PUFA supplement and n-3 PUFA supplement plus FG (n-3 PUFA + FG). n-3 PUFA + FG led to an increase in protein intake and a decrease in carbohydrate intake compared with n-3 PUFA (P < 0·02) in males and females. Sex-treatment interactions were observed for TAG (P = 0·03) and highly sensitive C-reactive protein (hsCRP) (P = 0·001) levels. In females, n-3 PUFA reduced plasma TAG by 8 % and n-3 PUFA + FG by 23 %, whereas in males, n-3 PUFA reduced plasma TAG by 25 % and n-3 PUFA + FG by 11 %. n-3 PUFA increased serum hsCRP by 13 % and n-3 PUFA + FG strongly reduced hsCRP by 40 % in males, whereas in females, n-3 PUFA reduced serum hsCRP by 6 % and n-3 PUFA + FG increased hsCRP by 20 %. In conclusion, supplementation with FG may enhance the lipid-lowering effect of marine n-3 PUFA in females and beneficially counteract the effect of n-3 PUFA on serum hsCRP in males. Further studies are needed to identify the sex-dependent mechanisms responsible for the divergent effects of FG on TAG and hsCRP levels in females and males, respectively.
OBJECTIVE: The purpose of this article was to compare the effects of cod protein to those of other animal proteins on insulin sensitivity in insulin-resistant human subjects. RESEARCH DESIGN AND METHODS: Insulin sensitivity (M/I) was assessed using a hyperinsulinemic-euglycemic clamp in 19 insulin-resistant subjects fed a cod protein diet and a similar diet containing lean beef, pork, veal, eggs, milk, and milk products (BPVEM) for 4 weeks in a crossover design study. Both diets were formulated to differ only in protein source, thus providing equivalent amounts of dietary fibers and monounsaturated, polyunsaturated (including n-3), and saturated fatty acids (1.1:1.8:1.0). Beta-cell function, estimated by oral glucose tolerance test-derived parameters, was also assessed. RESULTS: There was a significant improvement in insulin sensitivity (P = 0.027) and a strong tendency for a better disposition index (beta-cell function x M/I) (P = 0.055) in subjects consuming the cod protein diet compared with those consuming the BPVEM diet. When median baseline M/I (4.8 x 10(-3) mg x kg(-1) x min(-1) x pmol(-1)) was taken into account, an interaction on the 30-min C-peptide-to-30-min glucose ratio, used as an index of beta-cell function, was observed between diet and M/I status (P = 0.022). Indeed, this ratio strongly tended to increase in subjects with low M/I consuming the cod protein diet compared with those consuming the BPVEM diet (P = 0.065). CONCLUSIONS: Dietary cod protein improves insulin sensitivity in insulin-resistant individuals and thus could contribute to prevention of type 2 diabetes by reducing the metabolic complications related to insulin resistance.