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Intimate partner relationship quality during the child-bearing years has implications for maternal health. The purpose of this study was to test whether partner satisfaction, partner conflict, and their interaction predicted maternal cardio-metabolic health at 12-months postpartum. Women were recruited in 5 U.S. sites. Partner conflict and satisfaction were measured at 6-months postpartum, and cardio-metabolic indicators (blood pressure, waist-hip ratio, glycosylated hemoglobin, total cholesterol:HDL ratio) were assessed at 6- and 12-months. Cardio-metabolic indices were scored continuously (CM risk) and using clinical risk cutoffs (CM scores). A significant conflict-by-satisfaction interaction emerged for the CM risk, b(SE) = .043 (.016), p = .006, and CM scores, b(SE)= .089 (.028), p = .002, such that when partner satisfaction was low, low partner conflict was associated with poorer postpartum cardio-metabolic health. This is the first study to examine close relationships and cardio-metabolic health during the child-bearing years, an issue warranting further attention., Author(s): Kharah M. Ross [sup.1] , Christine Guardino [sup.1] , Calvin J. Hobel [sup.2] , Christine Dunkel Schetter [sup.1] Author Affiliations: (Aff1) 0000 0000 9632 6718, grid.19006.3e, Department of Psychology, [...]

This study aimed to investigate effects of curcumin on high fructose diet (HFD)-induced metabolic syndrome (MetS) in rats and the possible mechanisms involved. MetS was induced in male albino rats (n = 20), over 8 weeks, by 65% HFD. For 8-week experiment period, rats were assigned to 2 equal groups: curcumin-treated rats received curcumin (200 mg/kg, p.o, once daily) along with HFD, and untreated rats were fed with HFD only. We evaluated body mass (BM), systolic blood pressure (SBP), homeostasis model assessment of insulin resistance (HOMA-IR), and serum levels of glucose, insulin, leptin, total cholesterol (TC), triglycerides (TGs), uric acid, malondialdehyde (MDA; lipid peroxidation product), and tumor necrosis factor-α (TNF-α; inflammatory cytokine), and serum catalase (endogenous antioxidant) activity and immunohistochemical expression of nuclear factor κB (NF-κB; inflammation-related transcription factor) in hepatocytes. HFD produced increases in BM, SBP, HOMA-IR, and serum levels of glucose, insulin, leptin, TC, TGs, uric acid, MDA, and TNF-α, a decrease in catalase activity, and strong positive expression of NF-κB in hepatocytes. Curcumin, in presence of HFD, produced significant improvements in all glucose and fat metabolism parameters, and in oxidative stress and inflammation biomarkers. Curcumin may potentially be useful in the treatment of MetS through its ability to modulate oxidation stress status and inflammation cascades. Key words: curcumin, fructose, metabolic syndrome, insulin resistance, rats. Cette etude visait a examiner les effets de la curcumine sur le syndrome metabolique (SMet) induit par une diete riche en fructose (DRF) chez le rat et les mecanismes possiblement impliques. Le SMet a ete induit chez des rats albinos males (n = 20) pendant 8 semaines par une DRF a 65 %. Pendant les 8 semaines d'experimentation, les rats ont ete repartis en 2 groupes egaux: traite a la curcumine : administration de curcumine (200 mg/kg, p.o., une fois par jour) avec la DRF et groupe non traite : nourri a la DRF seulement. Les auteurs ont evalue le poids corporel (PC), la tension arterielle systolique (TAS), l'indice de resistance a l'insuline HOMA-IR, et les niveaux seriques de glucose, d'insuline, de leptine, de cholesterol total (CT), de triglycerides (TG), d'acide urique, de malonaldehyde (MDA; produit de peroxydation lipidique), et du facteur necrosant des tumeurs-α (TNF-α; cytokine inflammatoire), de meme l'activite de la catalase dans le serum (antioxydant endogene) et l'expression par immunohistochimie du facteur NF-κB (facteur de transcription lie a l'inflammation) dans les hepatocytes. La DRF provoquait des augmentations du PC, de la TAS, de l'indice HOMA-IR, et des niveaux seriques de du glucose, d'insuline, de la leptine, du CT, des TG, de l'acide urique, du MDA et du TNF-α, une diminution de l'activite de la catalase et une forte expression du NF-κB dans les hepatocytes. La curcumine, en presence de la DRF, ameliorait significativement tous les parametres lies au metabolisme du glucose et des lipides, et des biomarqueurs du stress oxydant et de l'inflammation. La curcumine peut potentiellement etre utile dans le traitement du SMet par sa capacite de moduler le stress oxydant et les cascades inflammatoires. [Traduit par la Redaction] Mots-cles: curcumine, fructose, syndrome metabolique, resistance a l'insuline, rats., Introduction Metabolic syndrome (MetS) is a cluster of metabolic features including central obesity, insulin resistance, dyslipidemia, and hypertension. These features commonly predispose individuals to high risk of morbidities (e.g., type [...]

Dipeptidyl peptidase 4 (DPP-4) inhibitors are widely used antihyperglycemic agents for type 2 diabetes mellitus. Recently, increasing attention has been focused on the pleiotropic actions of DPP-4 inhibitors. The aim of the present study was to examine whether gemigliptin, a recently developed DPP-4 inhibitor, could ameliorate features of metabolic syndrome. Mice were fed a Western diet (WD) for 12 weeks and were subsequently divided into 2 groups: mice fed a WD diet alone or mice fed a WD diet supplemented with gemigliptin for an additional 4 weeks. Gemigliptin treatment attenuated WD-induced body mass gain, hypercholesterolemia, adipocyte hypertrophy, and macrophage infiltration into adipose tissue, which were accompanied by an increased expression of uncoupling protein 1 in subcutaneous fat. These events contributed to improved insulin sensitivity, as assessed by the homeostasis model assessment of insulin resistance and intraperitoneal insulin tolerance test. Furthermore, gemigliptin reduced WD-induced hepatic triglyceride accumulation via inhibition of de novo lipogenesis and activation of fatty acid oxidation, which was accompanied by AMP-dependent protein kinase activation. Gemigliptin ameliorated WD induced hepatic inflammation and fibrosis through suppression of oxidative stress. These results suggest that DPP-4 inhibitors may represent promising therapeutic agents for metabolic syndrome beyond their current role as antihyperglycemic agents. Key words: DPP-4 inhibitor, metabolic syndrome, Western diet, adipocyte hypertrophy, adipose inflammation, nonalcoholic steatohepatitis, AMP-dependent protein kinase, oxidative stress. Les inhibiteurs de la dipeptidyl peptidase 4 (DPP-4) sont largement utilises comme agents anti-hyperglycemiques dans le diabete sucre de type 2. Recemment, une grande attention a ete portee aux actions pleiotropes des inhibiteurs de la DPP-4. Le but de la presente etude etait d'examiner si la gemigliptine, un inhibiteur de la DPP-4 recemment developpe, pouvait ameliorer les caracteristiques du syndrome metabolique. Des souris ont ete nourries avec un regime alimentaire occidental (RAO) pendant 12 semaines et subsequemment reparties en deux groupes : souris nourries avec un RAO seul ou souris nourries avec un RAO supplemente a la gemigliptine pendant 4 semaines de plus. Le traitement a la gemigliptine attenuait le gain de poids corporel, l'hypercholesterolemie, l'hypertrophie des adipocytes et l'infiltration du tissu adipeux par les macrophages resultant de le RAO, qui etaient accompagnes par une expression accrue de la thermogenine dans le gras sous-cutane. Ces evenements contribuaient a l'amelioration de la sensibilite a l'insuline, telle qu'estimee par revaluation du modele d'homeostasie de la resistance a l'insuline (HOMA;<< homeostasis model assessment of insuline resistance >>) et par le test de tolerance a l'insuline intraperitoneale. De plus, la gemigliptine reduisait l'accumulation de triglycerides hepatiques induite par le RAO par l'inhibition de la lipogenese de novo et l'activation de l'oxydation des acides gras, qui etait accompagnee par l'activation de la proteine kinase dependante de l'AMP. La gemigliptine ameliorait l'inflammation hepatique et la fibrose induites par le RAO par la suppression du stress oxydant. Ces resultats suggerent que les inhibiteurs de la DPP-4 peuvent constituer des agents therapeutiques prometteurs pour traiter le syndrome metabolique, au-dela de leurs roles actuels comme agents anti- hyperglycemiques. [Traduit par la Redaction] Mots-cles: inhibiteur de la DPP-4, syndrome metabolique, regime alimentaire occidental, hypertrophie des adipocytes, inflammation adipeuse, steatose hepatique non alcoolique, proteine kinase dependante de l'AMP, stress oxydant., Introduction Metabolic syndrome is a cluster of clinical features including central obesity, dyslipidemia, hypertension, and hyperglycemia (Eckel et al. 2005). The pathogenesis of metabolic syndrome is complex and poorly understood, [...]

ARTICLE INFO Keywords: Ovariectomized rats Metabolic Syndrome Fat tissue Cholesterol Joint cartilage Cimicifuga racemosa ABSTRACT Purpose: An unphysiologic accumulation of fat cells in many parts of the body including abdomen [...]

Exercise has beneficial effects on human health, including protection against metabolic disorders such as diabetes (1). However, the cellular mechanisms underlying these effects are incompletely understood. The lysosomal degradation pathway, autophagy, is an intracellular recycling system that functions during basal conditions in organelle and protein quality control (2). During stress, increased levels of autophagy permit cells to adapt to changing nutritional and energy demands through protein catabolism (3). Moreover, in animal models, autophagy protects against diseases such as cancer, neurodegenerative disorders, infections, inflammatory diseases, ageing and insulin resistance (4-6). Here we show that acute exercise induces autophagy in skeletal and cardiac muscle of fed mice. To investigate the role of exercise-mediated autophagy in vivo, we generated mutant mice that show normal levels of basal autophagy but are deficient in stimulus (exercise- or starvation)-induced autophagy. These mice (termed BCL2 AAA mice) contain knock-in mutations in BCL2 phosphorylation sites (Thr69Ala, Ser70Ala and Ser84Ala) that prevent stimulus-induced disruption of the BCL2-beclin-1 complex and autophagy activation. BCL2 AAA mice show decreased endurance and altered glucose metabolism during acute exercise, as well as impaired chronic exercise-mediated protection against high-fat-diet-induced glucose intolerance. Thus, exercise induces autophagy, BCL2 is a crucial regulator of exercise- (and starvation)induced autophagy in vivo, and autophagy induction may contribute to the beneficial metabolic effects of exercise., To investigate whether autophagy is induced by exercise, we analysed tissues of mice that transgenically express a green fluorescent protein (GFP)-labelled marker of autophagosomes, GFP-LC3 (LC3 is also known as [...]

Aging is a major risk factor for metabolic disease and loss of skeletal muscle mass and strength, a condition known as sarcopenia. Both conditions present a major health burden to the elderly population. Here, we analyzed the effect of mildly increased PGC-1[alpha] expression in skeletal muscle during aging. We found that transgenic MCK-PGC-1[alpha] animals had preserved mitochondrial function, neuromuscular junctions, and muscle integrity during aging. Increased PGC-1[alpha] levels in skeletal muscle prevented muscle wasting by reducing apoptosis, autophagy, and proteasome degradation. The preservation of muscle integrity and function in MCK-PGC-1[alpha] animals resulted in significantly improved whole-body health; both the loss of bone mineral density and the increase of systemic chronic inflammation, observed during normal aging, were prevented. Importantly, MCK-PGC-1[alpha] animals also showed improved metabolic responses as evident by increased insulin sensitivity and insulin signaling in aged mice. Our results highlight the importance of intact muscle function and metabolism for whole-body homeostasis and indicate that modulation of PGC-1[alpha] levels in skeletal muscle presents an avenue for the prevention and treatment of a group of age-related disorders. mitochondria | PGC-1[alpha] www.pnas.org/cgi/doi/10.1073/pnas.0911570106

Animals are remarkably efficient in absorbing dietary fat and assimilating this energy-dense nutrient into the white adipose tissue (WAT) for storage. Although this metabolic efficiency may confer an advantage in times of calorie deprivation, it contributes to obesity and associated metabolic disorders when dietary fat is abundant (1,2). Here we show that the intestinal lipid synthesis enzyme acyl CoA:monoacylglycerol acyltransferase-2 (MGAT2) has a crucial role in the assimilation of dietary fat and the accretion of body fat in mice. Mice lacking MGAT2 have a normal phenotype on a low-fat diet. However, on a high-fat diet, MGAT2-deficient mice are protected against developing obesity, glucose intolerance, hypercholesterolemia and fatty livers. Caloric intake is normal in MGAT2-deficient mice, and dietary fat is absorbed fully. However, entry of dietary fat into the circulation occurs at a reduced rate. This altered kinetics of fat absorption apparently results in more partitioning of dietary fat toward energy dissipation rather than toward storage in the WAT. Thus, our studies identify MGAT2 as a key determinant of energy metabolism in response to dietary fat and suggest that the inhibition of this enzyme may prove to be a useful strategy for treating obesity and other metabolic diseases associated with excessive fat intake., Dietary fat, as triacylglycerol, is a major source of calories, accounting for over 30% of daily intake in most developed countries (3). The assimilation of triacylglycerol as body fat is [...]

The epidemic emergence of modern chronic diseases largely stems from the adoption of a sedentary lifestyle and excess energy intake. However, it has long been known that regular physical activity induces multiple adaptations within skeletal muscle and other organs and these adaptations have positive outcomes for the prevention and treatment of many metabolic disorders. In recognition of such benefits, a recent goal of industry-funded research is to discover orally active compounds that mimic the effects of exercise training, so-called 'exercise pills' This article provides an overview of the role of skeletal muscle in health and disease and discusses whether 'exercise mimetics' have any potential to combat metabolic diseases.

The refeeding syndrome is a potentially lethal complication of refeeding in patients who are severely malnourished from whatever cause. Too rapid refeeding, particularly with carbohydrate may precipitate a number of metabolic and pathophysiological complications, which may adversely affect the cardiac, respiratory, haematological, hepatic and neuromuscular systems leading to clinical complications and even death. We aimed to review the development of the refeeding syndrome in a variety of situations and, from this and the literature, devise guidelines to prevent and treat the condition. We report seven cases illustrating different aspects of the refeeding syndrome and the measures used to treat it. The specific complications encountered, their physiological mechanisms, identification of patients at risk, and prevention and treatment are discussed. Each case developed one or more of the features of the refeeding syndrome including deficiencies and low plasma levels of potassium, phosphate, magnesium and thiamine combined with salt and water retention. These responded to specific interventions. In most cases, these abnormalities could have been anticipated and prevented. The main features of the refeeding syndrome are described with a protocol to anticipate, prevent and treat the condition in adults. doi:10.1038/sj.ejcn.1602854; published online 15 August 2007 Keywords: refeeding syndrome; hypophosphataemia; hypomagnesaemia; thiamine deficiency; nutritional therapy; guidelines, Introduction The refeeding syndrome was first reported among those released from concentration camps following the Second World War (Burger et al., 1948; Schnitker et al., 1951). Oral feeding of these [...]

The profession of dietetics can take an increasingly prominent role in managing health and patient care as clinicians gain access to three new resources: detailed information about the metabolic status of healthy individual clients, metabolic knowledge about the relationships between metabolite abundances and health, and bioinformatics tools that link clients' metabolism to their present and future health status. The current use of single biomarkers as indicators of disease will be replaced by comprehensive profiling of individual metabolites linked to an understanding of health and human metabolism--the emerging science now known as metabolomics. Industrial and academic initiatives are currently developing the analytical and bioinformatic technologies needed to assemble the quantitative reference databases of metabolites as the metabolic analog of the human genome. With these in place, dietetics professionals will be able to assess both the current health status of individuals and predict their health trajectories. Another important role for dietetics professionals will be to assist in the development of the tools and their application in predicting how an individual's specific metabolic pattern can be changed by diet, drugs, and lifestyle, with the goal of improving health and preventing the development of chronic diseases. J Am Diet Assoc. 2005;105:1425-1432.

Byline: V. Soumya, Y. Muzib, P. Venkatesh Objective: To evaluate the potential effect of bamboo seed oil in decreasing the major metabolic symptoms associated with letrozole-induced polycystic ovarian disease using [...]

The authors discuss the role of highly active antiretroviral therapy in creating a risk of cardiovascular diseases in HIV-infected patients. Results demonstrate the development of metabolic abnormalities in these patients which may cause diabetes, stroke and cardiovascular diseases.