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A Single Bout of Premeal Resistance Exercise Improves Postprandial Glucose Metabolism in Obese Men with Prediabetes.
Bittel, AJ, Bittel, DC, Mittendorfer, B, Patterson, BW, Okunade, AL, Abumrad, NA, Reeds, DN, Cade, WT
Medicine and science in sports and exercise. 2021;53(4):694-703
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Prediabetes is a metabolic condition defined by elevated fasting (impaired fasting glucose) and/or postprandial (impaired glucose tolerance) plasma glucose. The aim of this study was to determine the effects of a single bout of resistance exercise on postprandial glucose metabolism following a mixed meal in obese, sedentary men with prediabetes. This study is a randomised, cross-over study design which enrolled ten participants. Participants were aged 39-62 years, obese, and demonstrated insulin resistance with compensatory increases in beta cell function. Results show that a single bout of resistance exercise performed 4.5 hours before a mixed meal (as opposed to an oral glucose tolerance test) reduced total postprandial glucose appearance, increased insulin sensitivity, and reduced the glycaemic response to a mixed meal. However, it did not have effect on glucose oxidation in obese men with prediabetes. Improvements in insulin sensitivity were complemented by reduced postprandial insulin concentration. Authors conclude that further investigation is needed to elucidate how resistance exercise affects exogenous (meal) vs endogenous postprandial glucose metabolism, and if additional bouts of exercise (i.e. training) produce superior outcomes for this population.
Abstract
INTRODUCTION Prediabetes is a major risk factor for type 2 diabetes and cardiovascular diseases. Although resistance exercise (RE) is recommended for individuals with prediabetes, the effects of RE on postprandial glucose metabolism in this population are poorly understood. Therefore, the purpose of this study was to elucidate how RE affects postprandial glucose kinetics, insulin sensitivity, beta cell function, and glucose oxidation during the subsequent meal in sedentary men with obesity and prediabetes. METHODS We studied 10 sedentary men with obesity (body mass index, 33 ± 3 kg·m-2) and prediabetes by using a randomized, cross-over study design. After an overnight fast, participants completed either a single bout of whole-body RE (seven exercises, 3 sets of 10-12 repetitions at 80% one-repetition maximum each) or an equivalent period of rest. Participants subsequently completed a mixed meal test in conjunction with an intravenous [6,6-2H2]glucose infusion to determine basal and postprandial glucose rate of appearance (Ra) and disappearance (Rd) from plasma, insulin sensitivity, and the insulinogenic index (a measure of beta cell function). Skeletal muscle biopsies were obtained 90 min postmeal to evaluate pyruvate-supported and maximal mitochondrial respiration. Whole-body carbohydrate oxidation was assessed using indirect calorimetry. RESULTS RE significantly reduced the postprandial rise in glucose Ra and plasma glucose concentration. Postprandial insulin sensitivity was significantly greater after RE, whereas postprandial plasma insulin concentration was significantly reduced. RE had no effect on the insulinogenic index, postprandial pyruvate respiration, or carbohydrate oxidation. CONCLUSION/INTERPRETATION A single bout of RE has beneficial effects on postprandial glucose metabolism in men with obesity and prediabetes by increasing postprandial insulin sensitivity, reducing the postprandial rise in glucose Ra, and reducing postprandial plasma insulin concentration.
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The effect of different sources of fish and camelina sativa oil on immune cell and adipose tissue mRNA expression in subjects with abnormal fasting glucose metabolism: a randomized controlled trial.
de Mello, VD, Dahlman, I, Lankinen, M, Kurl, S, Pitkänen, L, Laaksonen, DE, Schwab, US, Erkkilä, AT
Nutrition & diabetes. 2019;9(1):1
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Dietary fish oils, particularly omega-3 fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) found in oily fish, nuts and seeds have long been researched and purported to have both anti-inflammatory and glucose-stabilising effects when consumed orally and it is widely believed that in reducing low-grade inflammation and stabilising blood glucose levels, the risk of suffering from type 2 diabetes, heart disease or a stroke is reduced. Lean fish on the other hand has been far less researched with regards to its protective effects. This study was a randomised controlled study designed to assess and compare the protective effects of fish oils and Camelina Sativa oil (CSO - a seed oil containing alpha-linolenic acid) on inflammatory-related genes in subjects with suggestive pre-diabetes. Subjects were allocated to a randomised group and instructed to consume a given amount of either fatty fish, lean fish, camelina oil, or no fish/oil (control group). The study was carried out on 72 participants over a 12-week period. Although no significant change could be seen on inflammatory gene expression for the group consuming fatty fish, there was a modest decrease in inflammatory gene markers in the group consuming lean fish and a significant decrease in the group consuming CSO. Implications from this study suggest that CSO exerts its protective effect by reducing inflammation, therefore possibly decreasing the risk of strokes and cardiovascular episodes. The authors suggest that consuming a variety of fish, especially lean fish 4 times/ week could also play a protective role in cardiovascular health and type 2 diabetes.
Abstract
BACKGROUND/OBJECTIVES Molecular mechanisms linking fish and vegetable oil intakes to their healthy metabolic effects may involve attenuation of inflammation. Our primary aim was to examine in a randomized controlled setting whether diets enriched in fatty fish (FF), lean fish (LF) or ALA-rich camelina sativa oil (CSO) differ in their effects on the mRNA expression response of selected inflammation-related genes in peripheral blood mononuclear cells (PBMCs) and subcutaneous adipose tissue (SAT) in subjects with impaired fasting glucose. SUBJECTS/METHODS Samples from 72 participants randomized to one of the following 12-week intervention groups, FF (n = 19), LF (n = 19), CSO (n = 17) or a control group (n = 17), were available for the PBMC study. For SAT, 39 samples (n = 8, n = 10, n = 9, n = 12, respectively) were available. The mRNA expression was measured at baseline and 12 weeks by TaqMan® Low Density Array. RESULTS In PBMCs, LF decreased ICAM1 mRNA expression (P < 0.05), which was different (P = 0.06, Bonferroni correction) from the observed increase in the FF group (P < 0.05). Also, compared to the control group, LF decreased ICAM1 mRNA expression (P < 0.05). Moreover, the change in ICAM1 mRNA expression correlated positively with the intake of FF (P < 0.05) and negatively with the intake of LF (P < 0.05), independently of study group. A diet enriched in CSO, a rich source of alpha-linolenic acid (ALA), decreased PBMC IFNG mRNA expression (P < 0.01). The intake of CSO in the CSO group, but not the increase in plasma ALA proportions, correlated inversely with the IFNG mRNA expression in PBMCs (P = 0.08). In SAT, when compared with the control group, the effect of FF on decreasing IL1RN mRNA expression was significant (P < 0.03). CONCLUSION We propose that CSO intake may partly exert its benefits through immuno-inflammatory molecular regulation in PBMCs, while modulation of ICAM1 expression, an endothelial/vascular-related gene, may be more dependent on the type of fish consumed.
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Spexin peptide is expressed in human endocrine and epithelial tissues and reduced after glucose load in type 2 diabetes.
Gu, L, Ma, Y, Gu, M, Zhang, Y, Yan, S, Li, N, Wang, Y, Ding, X, Yin, J, Fan, N, et al
Peptides. 2015;71:232-9
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Little is known about the functions of the peptide spexin. Recent studies have shown a relationship between spexin and body weight regulation. It is thought that spexin might be related to glucose control and fat metabolism in type 2 diabetes mellitus (T2DM). The aim of this study was to examine the location of spexin in human tissue and measure spexin levels after a glucose load in T2DM patients. First, the researchers examined human tissue samples. Blood samples were then collected from 121 adults with T2DM and 105 healthy individuals. Additionally, an oral glucose tolerance test (OGTT) was performed on 12 healthy volunteers. In human tissue samples, the levels of spexin were highest in the adrenal gland, skin, stomach, small intestine, liver, thyroid, pancreatic islets, visceral fat, lung, colon, and kidney, and lowest in muscle and connective tissue. Blood levels of spexin were significantly lower in T2DM patients compared to healthy controls. Spexin levels were found to be inversely related to fasting blood glucose and lipids. During the OGTT, spexin levels were also inversely correlated with blood glucose levels. The authors concluded that spexin is highly expressed among endocrine and epithelial tissues. Changes in the blood levels of spexin could represent an adaptation to the rise of glucose and lipids associated with T2DM. However, the exact role of spexin in endocrine diseases is still to be discovered.
Abstract
Spexin mRNA and protein are widely expressed in rat tissues and associate with weight loss in rodents of diet-induced obesity. Its location in endocrine and epithelial cells has also been suggested. Spexin is a novel peptide that involves weight loss in rodents of diet-induced obesity. Therefore, we aimed to examine its expression in human tissues and test whether spexin could have a role in glucose and lipid metabolism in type 2 diabetes mellitus (T2DM). The expression of the spexin gene and immunoreactivity in the adrenal gland, skin, stomach, small intestine, liver, thyroid, pancreatic islets, visceral fat, lung, colon, and kidney was higher than that in the muscle and connective tissue. Immunoreactive serum spexin levels were reduced in T2DM patients and correlated with fasting blood glucose (FBG, r=-0.686, P<0.001), hemoglobin A1c (HbA1c, r=-0.632, P<0.001), triglyceride (TG, r=-0.236, P<0.001) and low density lipoprotein-cholesterol (LDL-C, r=-0.382, P<0.001). A negative correlation of blood glucose with spexin was observed during oral glucose tolerance test (OGTT). Spexin is intensely expressed in normal human endocrine and epithelial tissues, indicating that spexin may be involved in physiological functions of endocrine and in several other tissues. Circulating spexin levels are low in T2DM patients and negatively related to blood glucose and lipids suggesting that the peptide may play a role in glucose and lipid metabolism in T2DM.
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Enhanced cortisol production rates, free cortisol, and 11beta-HSD-1 expression correlate with visceral fat and insulin resistance in men: effect of weight loss.
Purnell, JQ, Kahn, SE, Samuels, MH, Brandon, D, Loriaux, DL, Brunzell, JD
American journal of physiology. Endocrinology and metabolism. 2009;296(2):E351-7
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Excess abdominal fat in men is a risk factor for both type 2 diabetes and cardiovascular disease. The aim of this study was to test the hypothesis that increased cortisol levels contribute to increased abdominal fat and insulin resistance in men. Twenty-four healthy men aged 18-70 took part in the study. Eight of the participants, who were obese, were put on a calorie-controlled weight loss diet. Cortisol production rate (CPR) and free cortisol (FC) were correlated with increased intra-abdominal fat (IAF) and decreased insulin sensitivity (Si). Cortisol levels were not correlated with subcutaneous fat (SQF). CPR and FC did not change with weight loss, suggesting that cortisol levels could influence the distribution of body fat upon weight regain. The authors concluded that their findings support a role for activation of the HPA axis and abnormal cortisol secretion in determining body fat distribution and predisposing these men to type 2 diabetes.
Abstract
Controversy exists as to whether endogenous cortisol production is associated with visceral obesity and insulin resistance in humans. We therefore quantified cortisol production and clearance rates, abdominal fat depots, insulin sensitivity, and adipocyte gene expression in a cohort of 24 men. To test whether the relationships found are a consequence rather than a cause of obesity, eight men from this larger group were studied before and after weight loss. Daily cortisol production rates (CPR), free cortisol levels (FC), and metabolic clearance rates (MCR) were measured by stable isotope methodology and 24-h sampling; intra-abdominal fat (IAF) and subcutaneous fat (SQF) by computed tomography; insulin sensitivity (S(I)) by frequently sampled intravenous glucose tolerance test; and adipocyte 11beta-hydroxysteroid dehydrogenase-1 (11beta-HSD-1) gene expression by quantitative RT-PCR from subcutaneous biopsies. Increased CPR and FC correlated with increased IAF, but not SQF, and with decreased S(I). Increased 11beta-HSD-1 gene expression correlated with both IAF and SQF and with decreased S(I). With weight loss, CPR, FC, and MCR did not change compared with baseline; however, with greater loss in body fat than lean mass during weight loss, both CPR and FC increased proportionally to final fat mass and IAF and 11beta-HSD-1 decreased compared with baseline. These data support a model in which increased hypothalamic-pituitary-adrenal activity in men promotes selective visceral fat accumulation and insulin resistance and may promote weight regain after diet-induced weight loss, whereas 11beta-HSD-1 gene expression in SQF is a consequence rather than cause of adiposity.