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 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The metabolic syndrome is a constellation of metabolic risk factors and physical conditions that are accompanied by an enhanced propensity toward the development of type 2 diabetes, atherosclerosis, and cardiovascular disease. It presents a combination of atherosclerosis risk including atherogenic dyslipidemia, hypertension, elevated plasma glucose, hypercoagulability, and a proinflammatory state. The 2 major underlying risk factors for the metabolic syndrome are obesity and insulin resistance. Exacerbating factors are physical inactivity, advancing age, and endocrine and genetic factors. Associated hyperinsulinemia, hyperglycemia, and elevated adipokine levels (adipose cytokines) lead to vascular endothelial dysfunction, an abnormal lipid profile, hypertension, and vascular inflammation, all of which promote the development of atherosclerotic cardiovascular disease. In this 2-part series, the authors present an up-to-date and detailed systematic review of the literature on this important topic.
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PMID:The metabolic syndrome and cardiovascular disease: Part I. 1860 51

Obstructive sleep apnea syndrome (OSAS) is related to the increased prevalence of cardiovascular disease and metabolic syndrome (MS). A novel adipokine, retinol binding protein-4 (RBP4), was reported to be associated with insulin resistance and the prevalence of type 2 diabetes. To examine whether plasma RBP4 is associated with insulin resistance and MS development in OSAS, we measured plasma RBP4 levels in 181 Japanese men (24 healthy controls and 40 mild, 64 moderate, and 53 severe OSAS) of whom 26 had mild glucose intolerance with HbA1c < or = 6.0%. After a full polysomnography, blood was collected between 06:00 and 07:00 AM. Plasma RBP4 levels in moderate/severe OSAS patients were higher than in control subjects. Plasma RBP4 was not correlated with apnea variables, HOMA-IR, or blood pressure. However, it was positively correlated with visceral fat areas and plasma triglyceride levels. The prevalence of MS was higher in severe OSAS patients than in mild/moderate OSAS and control subjects. Plasma RBP4 was higher in OSAS patients with MS than in those without MS. This study indicates that plasma RBP4 is associated with dyslipidemia, but not with insulin resistance, glucose intolerance, or hypertension in patients with OSAS. Visceral obesity may play key roles in increasing the plasma RBP4 level and MS development in OSAS.
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PMID:Visceral obesity is associated with the metabolic syndrome and elevated plasma retinol binding protein-4 level in obstructive sleep apnea syndrome. 1900 25

Obesity is a growing health problem in developed nations and in countries that are in the process of westernization like India. Obesity is linked with several health disorders such as hypertension and cardiovascular diseases, Type 2 diabetes, dyslipidemia and certain cancers. Currently, obesity-related malignancies, e.g., cancers of the breast, prostate and colon are the leading cancers in the industrialized societies. An increased amount of fat or adipose tissue in an overweight or obese person probably influences the development of cancer by releasing several hormone-like factors or adipokines. The majority of adipokines are pro-inflammatory, which promote pathological conditions like insulin resistance and cancer. On the other hand, many recent studies have shown that adiponectin, an anti-inflammatory adipokine, has anti-cancer and insulin-sensitizing effects. Adiponectin exerts its physiological functions chiefly by activation of AMP kinase via adiponectin receptors. Interestingly, several fruits and vegetables may contain adiponectin-like molecules or may increase the biosynthesis of adiponectin in our body. Studies on adiponectin analogues or adiponectin receptor agonists are a promising area of cancer chemoprevention research. In general, fruits and vegetables contain various dietary substances such as vitamins, minerals (like calcium and selenium), fiber and phytochemicals or phenolic compounds (like flavonoids and vanilloids), which may act as anti-cancer agents. Similarly, several dietary constituents including phytochemicals may have anti-obesity effects. Consumption of such dietary compounds along with caloric restriction and physical activity may be helpful in preventing obesity-related cancers. For this review article, we searched PubMed primarily to get the relevant literature.
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PMID:Dietary factors and cancer chemoprevention: an overview of obesity-related malignancies. 1924 81

Adrenomedullin (ADM) is a vasoactive peptide found to be related to obesity and its comorbidities: type 2 diabetes, hypertension, atherosclerosis, and coronary heart disease. ADM is increased both in plasma and in adipose tissue of obese individuals when compared to lean subjects and is considered as a member of the adipokine family. We determined plasma midregional proadrenomedullin (MR-proADM) concentrations in a cohort of 357 subjects with BMI ranging from 17.5 to 42.3 kg/m2 and no additional medical history. In parallel, 28 severely obese patients scheduled to undergo laparoscopic Roux-en-Y gastric bypass (RYGB) surgery were studied at two time points: before and 1 year after surgery. Outcome measurements were: MR-proADM, cortisol, leptin, C-reactive protein (CRP) thyroid-stimulating hormone (TSH), creatinine and metabolic parameters. BMI correlated significantly to plasma MR-proADM levels (r=0.714, P<0.001), also after adjustment for age and gender (r=0.767, P<0.001). In obese subjects, there was a positive relationship between MR-proADM and leptin (r=0.511, P=0.006). Following RYGB, plasma MR-proADM decreased from 0.76+/-0.03 to 0.62+/-0.02 pg/ml (P<0.0001). RYGB-induced changes in MR-proADM correlated significantly to changes in leptin (r=0.533, P=0.004) and in CRP (r=0.429, P=0.023). We conclude that BMI is an independent predictor of circulating MR-proADM levels. Weight loss after RYGB is associated with a significant decrease in plasma MR-proADM, which is related to surgery-induced changes in both circulating leptin and systemic inflammation.
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PMID:Plasma MR-proADM correlates to BMI and decreases in relation to leptin after gastric bypass surgery. 1924 78

The incidence of obesity has increased dramatically during recent decades. Obesity will cause a decline in life expectancy for the first time in recent history due to numerous co-morbid disorders. Adipocyte and adipose tissue dysfunction belong to the primary defects in obesity and may link obesity to several health problems including increased risk of insulin resistance, type 2 diabetes, fatty liver disease, hypertension, dyslipidemia, atherosclerosis, dementia, airway disease and some cancers. However, not all obese individuals develop obesity related metabolic or cardiovascular disorders potentially due to a preserved normal adipose tissue architecture and function. The majority of patients with obesity have an impaired adipose tissue function caused by the interaction of genetic and environmental factors which lead to adipocyte hypertrophy, hypoxia, a variety of stresses and inflammatory processes within adipose tissue. Ectopic fat accumulation including visceral obesity may be considered as a consequence of adipose tissue dysfunction, which is further characterized by changes in the cellular composition, increased lipid storage and impaired insulin sensitivity in adipocytes, and secretion of a proinflammatory, atherogenic, and diabetogenic adipokine pattern. This review focuses on the discussion of mechanisms causing or maintaining impaired adipose tissue function in obesity and potentially linking obesity to its associated disorders. A model is proposed how different pathogenic factors and mechanisms may cause dysfunction of adipose tissue.
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PMID:Adipose tissue dysfunction in obesity. 1935 89

White adipose tissue has traditionally been regarded as an organ of energy storage and mobilization. However, it is now recognized that this tissue is also an active endocrine organ that secretes a variety of signaling molecules termed adipokines. These adipokines have diverse autocrine-, paracrine-, and endocrine-like actions that impact a variety of biological and physiological processes, including adipocyte differentiation, local and systemic inflammation, overall energy balance, blood pressure, and glucose and lipid metabolism. Given the regulatory influence on these critical functions, dysregulation of adipokine secretion is believed to be a major contributor to obesity-related disorders such as hypertension, diabetes, and cardiovascular disease. Chemerin is a small, secreted protein that has been reported to serve as a chemoattractant for cells of the immune system such as macrophages and immature dendritic cells that express the cognate receptor chemokine-like receptor-1 (CMKLR1). Using adenoviral- delivered, short hairpin RNAs (shRNAs) to suppress chemerin or CMKLR1 expression, we have demonstrated a novel role for chemerin/CMKLR1 signaling as a positive regulator of adipocyte differentiation and metabolic function in the 3T3-L1 model of adipogenesis. This experimental approach provides an efficient and powerful means to characterize the functional roles of genes known to be involved in adipocyte formation and metabolism as well as to identify novel roles for genes in this model and/or other cells.
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PMID:Elucidation of chemerin and chemokine-like receptor-1 function in adipocytes by adenoviral-mediated shRNA knockdown of gene expression. 1944 31

Chromogranin A (CHGA/Chga), a proprotein, widely distributed in endocrine and neuroendocrine tissues (not expressed in muscle, liver, and adipose tissues), generates at least four bioactive peptides. One of those peptides, pancreastatin (PST), has been reported to interfere with insulin action. We generated a Chga knock-out (KO) mouse by the targeted deletion of the Chga gene in neuroendocrine tissues. KO mice displayed hypertension, higher plasma catecholamine, and adipokine levels and lower IL-6 and lipid levels compared with wild type mice. Liver glycogen content was elevated, but the nitric oxide (NO) level was diminished. Glucose, insulin, and pyruvate tolerance tests and hyperinsulinemic-euglycemic clamp studies established increased insulin sensitivity in liver but decreased glucose disposal in muscle. Despite higher catecholamine and ketone body levels and muscle insulin resistance, KO mice maintained euglycemia due to increased liver insulin sensitivity. Suppressed mRNA abundance of phosphoenolpyruvate carboxykinase and glucose-6-phosphatase (G6Pase) in KO mice further support this conclusion. PST administration in KO mice stimulated phosphoenolpyruvate carboxykinase and G6Pase mRNA abundance and raised the blood glucose level. In liver cells transfected with G6Pase promoter, PST caused transcriptional activation in a protein kinase C (PKC)- and NO synthase-dependent manner. Thus, PST action may be mediated by suppressing IRS1/2-phosphatidylinositol 3-kinase-Akt-FOXO-1 signaling and insulin-induced maturation of SREBP1c by PKC and a high level of NO. The combined effects of conventional PKC and endothelial NO synthase activation by PST can suppress insulin signaling. The rise in blood PST level with age and in diabetes suggests that PST is a negative regulator of insulin sensitivity and glucose homeostasis.
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PMID:A novel pathway of insulin sensitivity in chromogranin A null mice: a crucial role for pancreastatin in glucose homeostasis. 1970 99

BACKGROUND.: Reduced levels of serum adiponectin, an adipokine, are associated with cardiovascular and obesity-related diseases; however, relations between adiponectin and hypertension are unclear. METHODS.: This cross-sectional study examined adiponectin and ambulatory blood pressure monitoring (ABPM) in 33 pediatric renal transplant recipients (TXP), aged 8 to 19 years, median of 1.9 years after transplant. Serum total adiponectin (microg/mL) and high molecular weight-to-total adiponectin ratio (HMWr), 24-hr ABPM, and dual x-ray absorptiometry measures of fat mass were obtained. RESULTS.: The 12 TXP with hypertension (defined as BP index >1.0 and BP load >25%) had lower total adiponectin levels (7.4+/-3.2 vs. 10.9+/-5.2 microg/mL, P=0.045) compared with nonhypertensive TXP. Hypertensive TXP trended toward lower HMWr compared with nonhypertensive TXP (0.40+/-0.09 vs. 0.47+/-0.11, P=0.064). Levels did not differ according to sex, obesity or dipper status. In univariate analyses, total adiponectin and HMWr were negatively and significantly correlated with indexed BP in the daytime, nighttime, and 24-hr periods (R=-0.35 to -0.57). After adjustment for estimated glomerular filtration rate, fat mass, anti-hypertensive medication and fasting glucose, (1) lower total adiponectin was significantly and independently associated with greater elevations in all ABPM indexes except for nighttime systolic indexed BP, and (2) HMWr was inversely associated with all ABPM indexes. Lower adiponectin levels (P=0.049) and HMWr (P=0.042) were associated with greater odds of hypertension. CONCLUSION.: These data indicate that lower total adiponectin and HMWr were significantly and independently associated with greater ambulatory blood pressure.
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PMID:Serum adiponectin levels and ambulatory blood pressure monitoring in pediatric renal transplant recipients. 1985 50

It is well known that lifestyle-related diseases are closely related with not only environmental factors but also genetic factors. In addition, chronic lifestyle-related diseases, namely malignant neoplasm, cardiovascular diseases and cerebro-vascular diseases are the top three among the leading causes of death, and account for approximately 60% of mortality in Japan. Moreover, it is seriously concerned that dysregulation of adipokine secretion induced by visceral fat accumulation causes the clustering of various lifestyle-related diseases, followed by a marked increase in group with a high risk of contracting metabolic syndrome. Accordingly, it is an important issue to promote effective clinical examinations and health guidance with a focus on the prevention of metabolic syndrome including lifestyle-related diseases. In this review, I refer to 1) overview of lifestyle-related diseases such as hypertension, lipid metabolism disorders and diabetes, and metabolic syndrome in the national health and nutrition survey in Japan 2007, 2) useful clinical items for prevention of metabolic syndrome and those significances, 3) food for special dietary uses (FOSDU) and food with health claims (FHC) including food for specified health uses (FOSHU) and food with nutrient function claims (FNFC), 4) daily food or its functional component which may exert effective action such as hypolipidemic effect, and 5) prospects of clinical examination and study of food function. In conclusion, for prevention of lifestyle-related diseases, close relationship and mutual cooperation between clinical examination and food function study will be much more necessary in the future, which will contribute to the promotion of special health checkups and healthcare guidance focused on the prevention of metabolic syndrome.
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PMID:[The third function (regulation of physiological function) of food for prevention of lifestyle-related diseases--close linkage to clinical examination]. 2003 Jan 77

The activation of the sympathetic nervous system through the central actions of the adipokine leptin has been suggested as a major mechanism by which obesity contributes to the development of hypertension. However, direct evidence for elevated sympathetic activity in obesity has been limited to muscle. The present study examined the renal sympathetic nerve activity and cardiovascular effects of a high-fat diet (HFD), as well as the changes in the sensitivity to intracerebroventricular leptin. New Zealand white rabbits fed a 13.5% HFD for 4 weeks showed modest weight gain but a 2- to 3-fold greater accumulation of visceral fat compared with control rabbits. Mean arterial pressure, heart rate, and plasma norepinephrine concentration increased by 8%, 26%, and 87%, respectively (P<0.05), after 3 weeks of HFD. Renal sympathetic nerve activity was 48% higher (P<0.05) in HFD compared with control diet rabbits and was correlated to plasma leptin (r=0.87; P<0.01). Intracerebroventricular leptin administration (5 to 100 microg) increased mean arterial pressure similarly in both groups, but renal sympathetic nerve activity increased more in HFD-fed rabbits. By contrast, intracerebroventricular leptin produced less neurons expressing c-Fos in HFD compared with control rabbits in regions important for appetite and sympathetic actions of leptin (arcuate: -54%, paraventricular: -69%, and dorsomedial hypothalamus: -65%). These results suggest that visceral fat accumulation through consumption of a HFD leads to marked sympathetic activation, which is related to increased responsiveness to central sympathoexcitatory effects of leptin. The paradoxical reduction in hypothalamic neuronal activation by leptin suggests a marked "selective leptin resistance" in these animals.
Hypertension 2010 Apr
PMID:Exposure to a high-fat diet alters leptin sensitivity and elevates renal sympathetic nerve activity and arterial pressure in rabbits. 2019 95


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