Food temperature altered macronutrients induced changes in satiety hormones; glucagon - like peptide -1 and cholecystokinin and their correlation with subjective satiety.

BACKGROUND: The benefits of dietary macronutrients for weight management depend on the integrity of gut hormones. The role of food temperature in the release of satiety hormones and satiety needs elucidation. We aimed to determine the impact of different food temperatures with varying macronutrient compositions on satiety-related gut hormones glucagon-like peptide-1 (GLP-1) and cholecystokinin (CCK) and find the correlation of satiety hormones with appetite scores and remainder-day food (energy) intake. MATERIALS AND METHODS: Thirteen healthy participants (eight males and five females) aged 25-35 years with body mass index 18.5-24.9 kg/m2 with no medical illnesses or eating disorders consumed three compositions of meals (high carbohydrate, high fat, and high protein meals) each at three temperatures (cold, warm, and hot) in a randomized, double-blinded, controlled crossover design. Plasma concentrations of peptide hormones were determined at 0, 30, and 240 minutes by enzyme-linked immunosorbent assay, and 24-hours food recall was used for remainder-day food intake (remainder energy). Data were analyzed using SPSS version 27.0. The change in plasma levels of gut hormones with time was assessed using Friedman test; Kruskal-Wallis test was employed to compare GLP-1 and CCK hormonal levels across nine meals. RESULTS: A comparison of the three meals at the three temperatures (total of nine groups), showed that the GLP-1 and CCK plasma concentrations were significantly different (P < 0.001). GLP-1 and CCK responses increased more after hot meals than cold meals. Overall, high-fat meals had more effective gut hormone secretions. The area under the curve was increased for GLP-1 in high-fat meals and for CCK in hot meals. The peptide hormones (GLP-1 and CCK) were positively correlated with satiety scores and inversely with remainder food intake. CONCLUSION: The temperature of food was found to be an effective stimulus for the regulation of CCK and GLP-1 secretion. Hot food temperature increased satiety hormones (CCK and GLP-1), independent of food macronutrient composition.

Effect of short duration moderate intensity physical activity on glycemic control and antioxidant status of prediabetic population.

OBJECTIVES: To determine the effect of moderate-intensity physical activity on glycemic control and antioxidant status in the prediabetic population. METHODS: This experimental study was carried out in the Physiology Department, Institute of Basic Medical Sciences, Khyber Medical University, Peshawar, Pakistan. A total of 50 adult prediabetic subjects having 22 females and 28 males with the age range of 18 to 35 years were included. Diagnosis of prediabetes was made by glycated hemoglobin falling in the range of 5.7-6.4%, and impaired fasting glucose (100-125 mg/dL). Anthropometric measurements and biochemical assays were carried out at pre and post-exercise intervention. The participants performed moderate exercise of 30 min with heart rate max 7% ± 5% for 5 days a week for 8 weeks, monitored with pedometer. Enzyme-linked immunosorbent assay was carried out for individual and total antioxidants. RESULTS: Anthropometric parameters showed a significant decrease at post-exercise analysis. Similar changes were observed for fasting glucose (p<0.001) and glycated hemoglobin (p<0.001). Slight increase in uric acid (p<0.005) and total antioxidant concentration (p<0.001) were found. However, superoxide dismutase, glutathione peroxidase, vitamin C, and nitric oxide decreased (p<0.001). CONCLUSION: Moderate physical activity for 8 weeks significantly reduced the individual antioxidant levels, nominal increase in total antioxidant capacity and uric acid, and there was an explicit decline in the anthropometric and diabetic profile of prediabetic population.

Ghrelin is a persistent biomarker for chronic stress exposure in adolescent rats and humans.

Prolonged stressor exposure in adolescence enhances the risk of developing stress-sensitive mental illnesses, including posttraumatic stress disorder (PTSD), for many years following exposure cessation, but the biological underpinnings of this long-term vulnerability are unknown. We show that severe stressor exposure increased circulating levels of the hormone acyl-ghrelin in adolescent rats for at least 130 days and in adolescent humans for at least 4.5 years. Using a rodent model of longitudinal PTSD vulnerability in which rodents with a history of stressor exposure during adolescence display enhanced fear in response to fear conditioning administered weeks after stressor exposure ends, we show that systemic delivery of a ghrelin receptor antagonist for 4 weeks surrounding stressor exposure (2 weeks during and 2 weeks following) prevented stress-enhanced fear memory. These data suggest that protracted exposure to elevated acyl-ghrelin levels mediates a persistent vulnerability to stress-enhanced fear after stressor exposure ends.