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Introduction Metabolic disorders (e.g. diabetes, obesity, and metabolic syndrome) have over the past three decades reached pandemic dimensions, affecting a large number of the world population ( Wild & Byrne 2006 , Lin & Sun 2010 ). Insulin
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Institute of Biomedicine, University of Barcelona, Barcelona, Spain
Centro de Investigación Biomédica en Red de Obesidad y Nutrición (CIBEROBN), Carlos III Health Institute, Madrid, Spain
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Institute of Biomedicine, University of Barcelona, Barcelona, Spain
Centro de Investigación Biomédica en Red de Obesidad y Nutrición (CIBEROBN), Carlos III Health Institute, Madrid, Spain
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Department of Endocrinology and Nutrition, Hospital Clinic of Barcelona, Barcelona, Spain
Centro de Investigación Biomédica en Red de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM), Carlos III Health Institute, Madrid, Spain
Department of Medicine, Faculty of Medicine and Health Sciences, University of Barcelona, Barcelona, Spain
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exogenous prescribed GC treatment, induces a high cardiovascular and metabolic burden during active disease. Moreover, a long time after remission of hypercortisolism in endogenous CS, a metabolic syndrome-like phenotype persists with central obesity
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effects of NIC, maternal smoking in the critical period of lactation can be responsible for the future development of some components of the metabolic syndrome in progeny. Declaration of interest The authors declare that there is no conflict of interest
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characteristics of the metabolic syndrome including hypertriglyceridemia, hyperinsulinemia, and insulin resistance ( Johnson et al. 1991 ). Materials and Methods Animals and treatments Lean (Fa/?) and obese ( fa / fa
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Cancer Metabolism Research Group, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil
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95 1028 – 1037 . ( doi:10.1038/sj.bjc.6603360 ) Bjorndal B Burri L Staalesen V Skorve J Berge RK 2011 Different adipose depots: their role in the development of metabolic syndrome and mitochondrial response to hypolipidemic
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Center for Metabolic and Vascular Biology, Department of Pharmaceutical Sciences, Arizona State University, Tempe, Arizona 85287, USA
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Introduction Insulin regulates a wide variety of biological processes, and defects in insulin signaling in skeletal muscle are considered to be one of the main causes for a large number of disease conditions, such as insulin resistance, metabolic
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characteristics of the metabolic syndrome in women with polycystic ovary syndrome . Journal of Clinical Endocrinology and Metabolism 90 1929 – 1935 . ( https://doi.org/10.1210/jc.2004-1045 ) Baker BJ Akhtar LN & Benveniste EN 2009 SOCS1 and SOCS3 in the
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developing the metabolic syndrome including type 2 diabetes mellitus and hypertension ( Dunaif & Thomas 2001 , Elting et al. 2001 ). High circulating androgens in PCOS have been thought to originate from increased androgen generation in ovaries and
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Abstract
Pancreastatin is a regulatory peptide known to inhibit insulin secretion and insulin action with a glycogenolytic effect in the liver. This peptide is present in and secreted by many endocrine and chromaffin cells. Abnormalities of glucose, insulin and lipoprotein metabolism are common in patients with hypertension, as well as their first-degree relatives. We have recently studied a group of non-obese hypertensive subjects in which pancreastatin-like levels were increased compared with controls, and correlated with norepinephrine levels. We hypothesized that pancreastatin alongside the sympathoadrenal system might have a part in the insulin resistance of these patients, and this metabolic syndrome could play a role in the pathogenesis and complications of hypertension. In this article, we studied the normotensive offspring of these non-obese hypertensive patients and looked for metabolic abnormalities as well as plasma pancreastatin, glucagon and catecholamine levels. The subjects were separated into two groups: (1) offspring from non-insulin-resistant patients and (2) offspring from insulin-resistant patients. We found that after an intravenous glucose load, offspring from insulin-resistant patients were already hyperinsulinemic, although glucose clearance was normal, suggesting an early alteration in insulin sensitivity, whereas pancreastatin and catecholamine levels were normal compared with matched controls. However, offspring from non-insulin-resistant patients had no differences with controls. These results suggest that pancreastatin and catecholamines may not play an important role in triggering insulin resistance, although they may be important once the syndrome is established.
Journal of Endocrinology (1997) 153, 313–318
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The obese gene product, leptin, plays a central role in food intake and energy metabolism. The physiological roles of leptin in human bodily function have been broadened over the past decade since leptin was first discovered in 1994. Evidence has suggested that leptin plays a specific role in the intricate cascade of cardiovascular events, in addition to its well-established metabolic effects. Leptin, a hormone linking adiposity and central nervous circuits to reduce appetite and enhance energy expenditure, has been shown to increase overall sympathetic nerve activity, facilitate glucose utilization and improve insulin sensitivity. In addition, leptin is capable of regulating cardiac and vascular contractility through a local nitric oxide-dependent mechanism. However, elevated plasma leptin levels or hyperleptinemia, have been demonstrated to correlate with hyperphagia, insulin resistance and other markers of the metabolic syndrome including obesity, hyperlipidemia and hypertension, independent of total adiposity. Elevated plasma leptin levels may be an independent risk factor for the development of cardiovascular disease. Although mechanisms leading to hyperleptinemia have not been well described, factors such as increased food intake and insulin resistance have been shown to rapidly enhance plasma leptin levels and subsequently tissue leptin resistance. These findings have prompted the speculation that leptin in the physiological range may serve as a physiological regulator of cardiovascular function whereas elevated plasma leptin levels may act as a pathophysiological trigger and/or marker for cardiovascular diseases due to tissue leptin resistance.
