Postprandial Plasma Glucagon-like Peptide-1 Levels Research Articles

EFFECTS OF CHEWING TIME OF HIGH PROTEIN MEAL ON SATIETY AND GLP-1 HORMONE

Background: Chewing or mastication process affects satiety as well as satiety regulating hormone Glucagon-like Peptide-1 (GLP-1). Proteins have the highest satiating effects among the macronutrients. This study explored the association of chewing with satiety and GLP-1 in participants consuming high-protein meal. Methods: Fifteen healthy volunteers, aged 25-35 years were enrolled through random sampling. Effects of chewing on postprandial satiety and plasma GLP-1 was examined through quasi-experimental study conducted in Khyber Medical University, Peshawar, from Jan to Mar 2023. Three visits were designed with one week wash-out period. Satiety and GLP-1 were compared among normal, fast, and slow chewing conditions, while providing high protein meal. Subjective satiety was assessed via visual analogue scale (VAS) and labelled magnitude scale (LMS), while serum GLP-1 levels were analysed through ELISA at baseline, 30, 120 and 240 min in each visit. Results: The participants had a mean chewing time of 793.66±311 second at normal rate. Mean chewing time was decreased to 496.60±135.82 second during fast chewing, while significantly increased to 1459.66±400.83 second during slow chewing. A comparison of satiety at different chewing rates revealed that slow chewing significantly reduced hunger and enhanced fullness (p<0.05), relative to normal and fast chewing, at 240 minutes (p<0.05). However, no significant difference was observed in plasma GLP-1 levels at any time intervals (p>0.05). Conclusion: Satiety is significantly influenced by chewing and number of chews per bite of a high protein meal, whereas postprandial plasma GLP-1 levels show no significant differences across different chewing rates. Pak J Physiol 2024;20(2):31-35

Total gastrectomy-induced reductions in food intake and weight are counteracted by rikkunshito by attenuating glucagon-like peptide-1 elevation in rats

Decrease in appetite and weight after total gastrectomy in patients with gastric cancer leads to a decrease in quality of life, increased mortality, and may necessitate discontinuation of adjuvant chemotherapy. The aim of this study is to determine whether rikkunshito, a Japanese herbal medicine, increases food intake and weight after gastrectomy in rats. Male rats underwent gastrectomy followed by roux-en-Y reconstruction or sham operation and were then treated with rikkunshito for 14 days starting on postoperative day 3. Daily food intake, weight, plasma glucagon-like peptide-1 (GLP-1), and ghrelin levels were measured. A pilot study to measure pre- and postoperative plasma GLP-1 levels was conducted in patients who underwent total gastrectomy for gastric cancer. Administration of rikkunshito after gastrectomy in rats significantly increased food intake and weight, which continued for at least 2 weeks after treatment. Both fasting and postprandial plasma GLP-1 levels were increased markedly after gastrectomy compared with sham-operated animals. Increased GLP-1 levels in rats after gastrectomy were suppressed markedly by rikkunshito. rikkunshito had no significant effect on plasma ghrelin levels after gastrectomy. Treatment with a GLP-1 receptor antagonist significantly improved food intake and weight after gastrectomy. Plasma fasting GLP-1 levels in patients with gastric cancer were increased greatly after gastrectomy on postoperative day 1. Administration of rikkunshito suppresses plasma GLP-1 levels after total gastrectomy, which is associated with recovery from reduced food intake and weight in rats.

Effects of 24-week treatment with acarbose on glucagon-like peptide 1 in newly diagnosed type 2 diabetic patients: a preliminary report

BackgroundTreatment with the alpha-glucosidase inhibitor (AGI) acarbose is associated with a significant reduction the risk of cardiovascular events. However, the underlying mechanisms of this effect are unclear. AGIs were recently suggested to participate in stimulating glucagon-like peptide 1 (GLP-1) secretion. We therefore examined the effects of a 24-week treatment of acarbose on endogenous GLP-1, nitric oxide (NO) levels, nitric oxide synthase (NOS) activity, and carotid intima-media thickness (CIMT) in newly diagnosed patients with type 2 diabetes (T2D).MethodsBlood was drawn from 24 subjects (14 male, 10 female, age: 50.7 ± 7.36 years, BMI: 26.64 ± 3.38 kg/m2, GHbA1c: 7.00 ± 0.74%) with drug-naïve T2D at 0 and 120 min following a standard mixed meal for the measurements of active GLP-1, NO and NOS. The CIMT was measured prior to and following 24 weeks of acarbose monotherapy (mean dose: 268 mg daily).ResultsFollowing 24 weeks of acarbose treatment, both fasting and postprandial plasma GLP-1 levels were increased. In patients with increased postprandial GLP-1 levels, serum NO levels and NOS activities were also significantly increased and were positively related to GLP-1 levels. Although the CIMT was not significantly altered following treatment with acarbose, a decreased CIMT was negatively correlated with increased GLP-1 levels.ConclusionsTwenty-four weeks of acarbose monotherapy in newly diagnosed patients with T2D is associated with significantly increased levels of both fasting and postprandial GLP-1 as well as significantly increased NO levels and NOS activity for those patients in whom postprandial GLP-1 levels were increased. Therefore, the benefits of acarbose on cardiovascular risk may be related to its stimulation of GLP-1 secretion.

Abstract P307: A Novel Protective Effect of the Antidiabetic Drug Voglibose via GLP-1 Receptor in the Infarcted Heart

Glucagon-like peptide 1 (GLP-1) reportedly exerts a protective effect against cardiac ischemia. We hypothesized that the α-glucosidase inhibitor voglibose, an unabsorbable antidiabetic drug with cardioprotective effects, may act via stimulation of GLP-1 receptors. The results of the present study suggest oral administration of voglibose reduces myocardial infarct size and mitigates cardiac dysfunction in rabbits following 30 min of coronary occlusion and 48 h of reperfusion. Voglibose increased basal and postprandial plasma GLP-1 levels and reduced postprandial plasma glucose levels. The infarct size-reducing effect of voglibose was abolished by treatment with exendin(9–39), wortmannin, L-NAME or 5-HD, which inhibit GLP-1 receptors, PI3K, NOS and K ATP channels, respectively. Western blot analysis showed that treatment with voglibose upregulated myocardial expression of phospho-Akt, phospho-eNOS, phospho-ERK and HSP27 following myocardial infarction. The upregulation of phospho-Akt was inhibited by exendin(9–39) and wortmannin, while the upregulation of phospho-ERK and HSP27 was inhibited by wortmannin but not by exendin(9–39). These findings suggest that voglibose reduces myocardial infarct size through stimulation of GLP-1 receptors, activation of PI3K-Akt-eNOS and ERK pathways, and the opening of mitochondrial K ATP channels. These findings may provide new insight into therapeutic strategies for the treatment of diabetic patients with coronary artery disease.

Antidiabetic Drug Voglibose Is Protective Against Ischemia—Reperfusion Injury Through Glucagon-Like Peptide 1 Receptors and the Phosphoinositide 3-Kinase-Akt-Endothelial Nitric Oxide Synthase Pathway in Rabbits

Glucagon-like peptide 1 (GLP-1) reportedly exerts a protective effect against cardiac ischemia. We hypothesized that the alpha-glucosidase inhibitor voglibose, an unabsorbable antidiabetic drug with cardioprotective effects, may act through stimulation of GLP-1 receptors. The results of the present study suggest oral administration of voglibose reduces myocardial infarct size and mitigates cardiac dysfunction in rabbits after 30 minutes of coronary occlusion and 48 hours of reperfusion. Voglibose increased basal and postprandial plasma GLP-1 levels and reduced postprandial plasma glucose levels. The infarct size-reducing effect of voglibose was abolished by treatment with exendin(9-39), wortmannin, Nomega-nitro-L-arginine methylester, or 5-hydroxydecanoate), which inhibit GLP-1 receptors, phosphoinositide 3-kinase, nitric oxide synthase, and K(ATP) channels, respectively. Western blot analysis showed that treatment with voglibose upregulated myocardial levels of phospho-Akt, phosphoendothelial nitric oxide synthase after myocardial infarction. The upregulation of phospho-Akt was inhibited by exendin(9-39) and wortmannin. These findings suggest that voglibose reduces myocardial infarct size through stimulation of GLP-1 receptors, activation of the phosphoinositide 3-kinase-Akt-endothelial nitric oxide synthase pathways, and the opening of mitochondrial K(ATP) channels. These findings may provide new insight into therapeutic strategies for the treatment of patients with coronary artery disease.