Probiotic supplementation prevents high-fat, overfeeding-induced insulin resistance in human subjects

The purpose of the present study was to determine whether probiotic supplementation (Lactobacillus casei Shirota (LcS)) prevents diet-induced insulin resistance in human subjects. A total of seventeen healthy subjects were randomised to either a probiotic (n 8) or a control (n 9) group. The probiotic group consumed a LcS-fermented milk drink twice daily for 4 weeks, whereas the control group received no supplementation. Subjects maintained their normal diet for the first 3 weeks of the study, after which they consumed a high-fat (65 % of energy), high-energy (50 % increase in energy intake) diet for 7 d. Whole-body insulin sensitivity was assessed by an oral glucose tolerance test conducted before and after overfeeding. Body mass increased by 0·6 (se 0·2) kg in the control group (P0·05). Fasting plasma glucose concentrations increased following 7 d of overeating (control group: 5·3 (se 0·1) v. 5·6 (se 0·2) mmol/l before and after overfeeding, respectively, P0·05). These results suggest that probiotic supplementation may be useful in the prevention of diet-induced metabolic diseases such as type 2 diabetes

A single day of excessive dietary fat intake reduces whole-body insulin sensitivity: the metabolic consequence of binge eating

Consuming excessive amounts of energy as dietary fat for several days or weeks can impair glycemic control and reduce insulin sensitivity in healthy adults. However, individuals who demonstrate binge eating behavior overconsume for much shorter periods of time; the metabolic consequences of such behavior remain unknown. The aim of this study was to determine the effect of a single day of high-fat overfeeding on whole-body insulin sensitivity. Fifteen young, healthy adults underwent an oral glucose tolerance test before and after consuming a high-fat (68% of total energy), high-energy (78% greater than daily requirements) diet for one day. Fasting and postprandial plasma concentrations of glucose, insulin, non-esterified fatty acids, and triglyceride were measured and the Matsuda insulin sensitivity index was calculated. One day of high-fat overfeeding increased postprandial glucose area under the curve (AUC) by 17.1% (p < 0.0001) and insulin AUC by 16.4% (p = 0.007). Whole-body insulin sensitivity decreased by 28% (p = 0.001). In conclusion, a single day of high-fat, overfeeding impaired whole-body insulin sensitivity in young, healthy adults. This highlights the rapidity with which excessive consumption of calories through high-fat food can impair glucose metabolism, and suggests that acute binge eating may have immediate metabolic health consequences for the individual

Cow's milk as a post-exercise recovery drink: implications for performance and health

Post-exercise recovery is a multi-facetted process that will vary depending on the nature of the exercise, the time between exercise sessions and the goals of the exerciser. From a nutritional perspective, the main considerations are: (1) optimisation of muscle protein turnover; (2) glycogen resynthesis; (3) rehydration; (4) management of muscle soreness; (5) appropriate management of energy balance. Milk is approximately isotonic (osmolality of 280–290 mosmol/kg), and the mixture of high quality protein, carbohydrate, water and micronutrients (particularly sodium) make it uniquely suitable as a post-exercise recovery drink in many exercise scenarios. Research has shown that ingestion of milk post-exercise has the potential to beneficially impact both acute recovery and chronic training adaptation. Milk augments post-exercise muscle protein synthesis and rehydration, can contribute to post-exercise glycogen resynthesis, and attenuates post-exercise muscle soreness/function losses. For these aspects of recovery, milk is at least comparable and often out performs most commercially available recovery drinks, but is available at a fraction of the cost, making it a cheap and easy option to facilitate post-exercise recovery. Milk ingestion post-exercise has also been shown to attenuate subsequent energy intake and may lead to more favourable body composition changes with exercise training. This means that those exercising for weight management purposes might be able to beneficially influence post-exercise recovery, whilst maintaining the energy deficit created by exercise

Addition of sodium alginate and pectin to a carbohydrate-electrolyte solution does not influence substrate oxidation, gastrointestinal comfort, or cycling performance

Eight well-trained cyclists ingested 68 g·h-1 of a carbohydrate-electrolyte solution with sodium alginate and pectin (CHO-ALG) or a taste and carbohydrate-type matched carbohydrate-electrolyte solution (CHO) during 120 min cycling at 55% Wmax followed by a ~20 min time trial. V̇O2, V̇CO2 blood glucose concentration, substrate oxidation, gastrointestinal symptoms and time trial performance (CHO-ALG: 1219 ± 84 s, CHO: 1267 ± 102 s; P = 0.185) were not different between trials. Novelty bullet: • Inclusion of sodium alginate and pectin in a carbohydrate drink does not influence blood glucose, substrate oxidation, gastrointestinal comfort or performance in cyclists

Short-term, high-fat overfeeding impairs glycaemic control but does not alter gut hormone responses to a mixed meal tolerance test in healthy, normal-weight individuals

Obesity is undoubtedly caused by a chronic positive energy balance. However, the early metabolic and hormonal responses to overeating are poorly described. This study determined glycaemic control and selected gut hormone responses to nutrient intake before and after seven days of high-fat overfeeding. Nine healthy individuals (5 males, 4 females) performed a mixed meal tolerance test (MTT) before and after consuming a high-fat (65%) high-energy (+50%) diet for seven days. Measurements of plasma glucose, NEFA, acylated ghrelin, GLP-1, GIP and serum insulin were taken before (fasting) and at 30 minutes intervals throughout the 180 min MTT (postprandial). Body mass increased by 0.79 ± 0.14 kg after high-fat overfeeding (p < 0.0001), and BMI increased by 0.27 ± 0.05 kg/m2 (p = 0.002). High-fat overfeeding also resulted in an 11.6% increase in postprandial glucose AUC (p = 0.007) and a 25.9% increase in postprandial insulin AUC (p = 0.005). Acylated ghrelin, GLP-1 and GIP responses to the MTT were all unaffected by the high-fat, high-energy diet. These findings demonstrate that even brief periods of overeating are sufficient to disrupt glycaemic control. However, as the postprandial orexigenic (ghrelin) and anorexigenic/insulintropic (GLP-1 and GIP) hormone responses were unaffected by the diet intervention, it appears that these hormones are resistant to short-term changes in energy balance, and that they do not play a role in the rapid reduction in glycaemic control

24 h severe energy restriction impairs post-prandial glycaemic control in young, lean males

Intermittent energy restriction (IER) involves short periods of severe energy restriction interspersed with periods of adequate energy intake, and can induce weight loss. Insulin sensitivity is impaired by short-term, complete energy restriction, but the effects of IER are not well known. In randomised order, 14 lean men (age: 25 (SD 4) y; BMI: 24 (SD 2) kg·m-2; body fat: 17 (4) %) consumed 24 h diets providing 100% (10441 (SD 812) kJ; EB) or 25% (2622 (SD 204) kJ; ER) of estimated energy requirements, followed by an oral glucose tolerance test (OGTT; 75g glucose drink) overnight fasted. Plasma/ serum glucose, insulin, non-esterified fatty acids (NEFA), glucagon-like peptide-1 (GLP-1), glucose-dependant insulinotropic peptide (GIP) and fibroblast growth factor-21 (FGF21) were assessed before and after (0 h) each 24 h dietary intervention, and throughout the 2 h OGTT. Homeostatic model assessment of insulin resistance (HOMA2-IR) assessed the fasted response and incremental (iAUC) or total (tAUC) area under the curve were calculated during the OGTT. At 0 h, HOMA2-IR was 23% lower after ER compared to EB (P<0.05). During the OGTT, serum glucose iAUC (P<0.001) serum insulin iAUC (P<0.05) and plasma NEFA tAUC (P<0.01) were greater during ER, but GLP-1 (P=0.161), GIP (P=0.473) and FGF21 (P=0.497) tAUC were similar between trials. These results demonstrate that severe energy restriction acutely impairs postprandial glycaemic control in lean men, despite reducing HOMA2-IR. Chronic intervention studies are required to elucidate the long-term effects of IER on indices of insulin sensitivity, particularly in the absence of weight loss

Influence of hyper-energetic, high-fat feeding on circulating hepatokines in healthy men: a randomised crossover study [Abstract]

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Neutrophil microvesicles drive atherosclerosis by delivering <i>miR-155</i> to atheroprone endothelium

Neutrophils are implicated in the pathogenesis of atherosclerosis but are seldom detected in atherosclerotic plaques. We investigated whether neutrophil-derived microvesicles may influence arterial pathophysiology. Here we report that levels of circulating neutrophil microvesicles are enhanced by exposure to a high fat diet, a known risk factor for atherosclerosis. Neutrophil microvesicles accumulate at disease-prone regions of arteries exposed to disturbed flow patterns, and promote vascular inflammation and atherosclerosis in a murine model. Using cultured endothelial cells exposed to disturbed flow, we demonstrate that neutrophil microvesicles promote inflammatory gene expression by delivering miR-155, enhancing NF-κB activation. Similarly, neutrophil microvesicles increase miR-155 and enhance NF-κB at disease-prone sites of disturbed flow in vivo. Enhancement of atherosclerotic plaque formation and increase in macrophage content by neutrophil microvesicles is dependent on miR-155. We conclude that neutrophils contribute to vascular inflammation and atherogenesis through delivery of microvesicles carrying miR-155 to disease-prone regions

The effect of quantity and quality of dietary fat intake on subcutaneous white adipose tissue inflammatory responses

The global prevalence of obesity and obesity-associated cardiometabolic diseases is a significant public health burden. Chronic low-grade inflammation in metabolic tissues such as white adipose tissue (WAT) is linked to obesity and may play a role in disease progression. The overconsumption of dietary fat has been suggested to modulate the WAT inflammatory environment. It is also recognised that fats varying in degree of fatty acid (FA) saturation may elicit differential WAT inflammatory responses. This information has originated predominantly from animal or cell models and translation into humans in vivo remains limited. This review will summarise human intervention studies investigating the effect of dietary fat quantity and quality on subcutaneous WAT inflammation, with a specific focus on the toll like receptor 4 (TLR4)/nuclear factor-κB (NF-κB) and nucleotide-binding and oligomerisation domain-like receptor, leucine-rich repeat and pyrin domain-containing 3 (NLRP3) inflammasome molecular signalling pathways. Overall, firm conclusions are hard to draw regarding the effect of dietary fat quantity and quality on WAT inflammatory responses due to the heterogeneity of study designs, composition of the diets and participant cohorts recruited. Previous studies have predominantly focused on measures of WAT gene expression. It is suggested that future work includes measures of WAT total content and phosphorylation of proteins involved in TLR4/NF-κB and NLRP3 signalling as this is more representative of alterations in WAT physiological function. Understanding pathways linking intake of total fat and specific FAs with WAT metabolic-inflammatory responses may have important implications for public health by informing dietary guidelines aimed at cardiometabolic risk reduction<br

Impact of high-fat overfeeding on white adipose tissue and systemic metabolic and inflammatory responses [Abstract]

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