Texture and Digestion Properties of Cooked Rice and Rice Noodles

Rice varieties high in amylose content have low glycemic and insulin responses. Rice noodles are processed by extrusion from high amylose content rice, which may also have low glycemic and insulin responses. In this study, cooked rice and rice noodles processed from two high amylose content cultivars, Guangluai4 (GL4) and Zhenguiai (ZGA), were chosen for in vitro starch digestion evaluation. Apparent amylose content of cultivars (i.e., GL4-28.4% and ZGA-26.8%) and pasting properties except final viscosity were significantly different between the cultivars. In vitro starch digestion results showed that the glucose production rate in rice noodles was significantly slower than that in cooked rice by 65.7% and 42.0% in GL4 and ZGA, respectively. The main reason for low glucose production in rice noodles was active digestion duration longer in rice noodles than in cooked rice, which reflects the slow release of glucose during starch digestion. The texture of rice noodles in the GL4 and ZGA cultivars is 3 and 2.3 times harder than that of cooked rice, respectively. Thus digestive enzymes can hardly enter the interior of rice noodles for amylolysis. As a result, the digestion time of rice noodles is longer, and the release of glucose during digestion is slower than that of cooked rice. The slower release of glucose during rice noodle digestion may be beneficial for prolonging satiety and reducing food intake. Consequently, eating rice noodles may help in improving or preventing diabetes and obesity over time.

L-arabinose and D-xylose: sweet pentoses that may reduce postprandial glucose and insulin responses

Background: Diets inducing high fluctuations in plasma glucose levels are linked to type 2 diabetes. L-arabinose and D-xylose have been hypothesized to inhibit intestinal sucrase activity, delay sucrose digestion, and reduce glycaemic and insulinaemic responses. However, few human studies have assessed this using realistic foods. Objective: We investigated the effects of the addition of L-arabinose and D-xylose on glucose homeostasis using a fruit-based drink and the effect of L-arabinose using a muffin. Design: Fifteen males participated in two double-blind, randomized cross-over experiments. In experiment A, three drinks were tested: (1) L-arabinose, (2) D-xylose and (3) control drink. In experiment B, two muffins were tested: (1) L-arabinose and (2) control muffin. All products consisted of ~50 g available carbohydrates, and L-arabinose or D-xylose was added as 10% of sucrose. Pre- and post-ingestive plasma glucose and insulin levels were measured at fixed time points up to 180 min after consumption. Results: Glucose and insulin peaks were lower after the L-arabinose and D-xylose drink than the control drink (P < 0.01). After consumption of the muffin, glucose responses were not significantly different; however, the insulin peak and incremental area under the curve (iAUC) tended to be lower for the L-arabinose muffin. Conclusion: L-arabinose and D-xylose are functional ingredients that can potentially lower the post-ingestive glycaemic and insulinaemic responses when added to realistic foods. However, the efficacy of applying L-arabinose appears to depend on the food matrix. Addition of these compounds needs further testing in other foods and in other populations, such as pre-diabetics.

Insulin-mediated muscle microvascular perfusion and its phenotypic predictors in humans

Insulin increases muscle microvascular perfusion and enhances tissue insulin and nutrient delivery. Our aim was to determine phenotypic traits that foretell human muscle microvascular insulin responses. Hyperinsulinemic euglycemic clamps were performed in 97 adult humans who were lean and healthy, had class 1 obesity without comorbidities, or controlled type 1 diabetes without complications. Insulin-mediated whole-body glucose disposal rates (M-value) and insulin-induced changes in muscle microvascular blood volume (ΔMBV) were determined. Univariate and multivariate analyses were conducted to examine bivariate and multivariate relationships between outcomes, ΔMBV and M-value, and predictor variables, body mass index (BMI), total body weight (WT), percent body fat (BF), lean body mass, blood pressure, maximum consumption of oxygen (VO2max), plasma LDL (LDL-C) and HDL cholesterol, triglycerides (TG), and fasting insulin (INS) levels. Among all factors, only M-value (r = 0.23, p = 0.02) and VO2max (r = 0.20, p = 0.047) correlated with ΔMBV. Conversely, INS (r = − 0.48, p ≤ 0.0001), BF (r = − 0.54, p ≤ 0.001), VO2max (r = 0.5, p ≤ 0.001), BMI (r = − 0.40, p < 0.001), WT (r = − 0.33, p = 0.001), LDL-C (r = − 0.26, p = 0.009), TG (r = − 0.25, p = 0.012) correlated with M-value. While both ΔMBV (p = 0.045) and TG (p = 0.03) provided significant predictive information about M-value in the multivariate regression model, only M-value was uniquely predictive of ΔMBV (p = 0.045). Thus, both M-value and VO2max correlated with ΔMBV but only M-value provided unique predictive information about ΔMBV. This suggests that metabolic and microvascular insulin responses are important predictors of one another, but most metabolic insulin resistance predictors do not predict microvascular insulin responses.

GRK2 contributes to glucose mediated calcium responses and insulin secretion in pancreatic islet cells

Diabetes is a metabolic syndrome rooted in impaired insulin and/or glucagon secretory responses within the pancreatic islets of Langerhans (islets). Insulin secretion is primarily regulated by two key factors: glucose-mediated ATP production and G-protein coupled receptors (GPCRs) signaling. GPCR kinase 2 (GRK2), a key regulator of GPCRs, is reported to be downregulated in the pancreas of spontaneously obesogenic and diabetogenic mice (ob/ob). Moreover, recent studies have shown that GRK2 non-canonically localizes to the cardiac mitochondrion, where it can contribute to glucose metabolism. Thus, islet GRK2 may impact insulin secretion through either mechanism. Utilizing Min6 cells, a pancreatic ß-cell model, we knocked down GRK2 and measured glucose-mediated intracellular calcium responses and insulin secretion. Silencing of GRK2 attenuated calcium responses, which were rescued by pertussis toxin pre-treatment, suggesting a Gαi/o-dependent mechanism. Pancreatic deletion of GRK2 in mice resulted in glucose intolerance with diminished insulin secretion. These differences were due to diminished insulin release rather than decreased insulin content or gross differences in islet architecture. Furthermore, a high fat diet feeding regimen exacerbated the metabolic phenotype in this model. These results suggest a new role for pancreatic islet GRK2 in glucose-mediated insulin responses that is relevant to type 2 diabetes disease progression.

Frequency of Interruptions to Sitting Time: Benefits for Postprandial Metabolism in Type 2 Diabetes

<b>Purpose:</b> To determine whether interrupting sitting with brief bouts of simple resistance activities (SRAs) at different frequencies improves postprandial glucose, insulin and triglycerides in adults with medication-controlled type 2 diabetes (T2D). <p><b>Methods:</b> Participants [n=23, 10 females, Age: 62±8 y (mean±SD), BMI: 32.7 ± 3.5 kg^.m^-2] completed a three-armed randomized crossover trial (6-14 day washout): sitting uninterrupted for 7 h (SIT); sitting with 3-minute SRAs (half-squats, calf raises, gluteal contractions, and knee raises) every 30 minutes (SRA3); and, sitting with 6-minute SRAs every 60 minutes (SRA6). Net incremental areas under the curve (iAUC_net) for glucose, insulin, and triglycerides were compared between conditions.</p> <p><b>Results:</b> <a>Glucose and insulin 7 h iAUC_netwere attenuated significantly during SRA6 (glucose 17.0 mmol^.h^.L^-1, 95% CI 12.5, 21.4; insulin 1229 pmol^.h^.L^-1, 95% CI 982, 1538) when compared to SIT (glucose 21.4 mmol^.h^.L^-1, 95% CI 16.9, 25.8; insulin 1411 pmol^.h^.L^-1, 95% CI 1128, 1767; <i>P</i> < 0.05), and compared to SRA3 ( for glucose only; 22.1 mmol^.h^.L^-1, 95% CI 17.7, 26.6; <i>P </i>= 0.01) No significant differences in glucose or insulin iAUC_net were observed comparing SRA3 and SIT. There was no statistically significant effect of condition on triglyceride iAUC_net. </a></p> <p><b>Conclusion:</b> In adults with medication-controlled T2D, interrupting prolonged sitting with 6-minute SRAs every 60 minutes reduced postprandial glucose and insulin responses. Other frequencies of interruptions and potential longer-term benefits require examination to clarify clinical relevance. </p>

Effects of Totum-63 on glucose homeostasis and post-prandial glycemia: a translational study

Global prevalence of type 2 diabetes (T2D) is rising and may affect 700 million people by 2045. Totum-63 is a polyphenol-rich natural composition developed to reduce the risk of T2D. We first investigated the effects of Totum-63 supplementation in high-fat diet (HFD)-fed mice for up to 16 weeks, and thereafter assessed its safety and efficacy (2.5 g or 5 g per day) in 14 overweight men (mean age 51.5 years, BMI 27.6 kg.m-2) for 4 weeks. In HFD-fed mice, Totum-63 reduced body weight and fat mass gain while lean mass was unchanged. Moreover, fecal energy excretion was higher in Totum-63 supplemented mice, suggesting a reduction of calorie absorption in the digestive tract. In the gut, metagenomic analyses of fecal microbiota revealed a partial restoration of HFD-induced microbial imbalance, as shown by PCoA analysis of microbiota composition. HFD-induced increase in HOMA-IR score was delayed in supplemented mice, and insulin response to an OGTT was significantly reduced, suggesting that Totum-63 may prevent HFD-related impairments in glucose homeostasis. Interestingly, these improvements could be linked to restored insulin signaling in subcutaneous adipose tissue and soleus muscle. In the liver, HFD-induced steatosis was reduced by 40% (as shown by triglyceride content). In the subsequent study in men, Totum-63 (5g.day-1) improved glucose and insulin responses to a high-carbohydrate breakfast test (84% kcal carbohydrates). It was well tolerated, with no clinically significant adverse events reported. Collectively, these data suggest that Totum-63 could improve glucose homeostasis in both HFD-fed mice and overweight individuals, presumably through a multi-targeted action on different metabolic organs.