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Query: UMLS:C0948265 (metabolic syndrome)
 24,271 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The metabolic syndrome is associated with a marked increase in risk of type 2 diabetes and atherosclerotic vascular disease (AVD). The mechanism responsible for the metabolic syndrome is uncertain, but recent evidence suggests that a combination of low birth weight and adult obesity is associated with a markedly increased prevalence. Insulin resistance is the cardinal feature of the metabolic syndrome. Several hormones, have modes of action that either potentiate or reduce the biological actions of insulin and, therefore, attenuate or induce insulin resistance. Since insulin action may be modified, these hormones potentially contribute to the pathogenesis of the metabolic syndrome. The purpose of this review is to discuss programming of hormones that modulate insulin action. The review focuses on two major endocrine pathways: (i) glucocorticoid hormone action; and (ii) the growth hormone (GH)-insulin-like growth factor (IGF-1) axis, and discusses mechanisms linking abnormal activity of these pathways with reduced early growth, adult obesity and the metabolic syndrome.
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PMID:Programming other hormones that affect insulin. 1180 24

There are several potential cellular and molecular pathways whereby cardiovascular risk factors act through very specific signal transduction pathways in the formation of atherosclerosis, as seen often in the metabolic syndrome. Many examples point to multiple postreceptor defects in the insulin signaling pathway in vascular tissue, however, there are differences in the insulin receptor pathway in vascular tissue compared with skeletal muscle or fat. In addition to insulin receptors, insulin may affect atherosclerotic changes in the vascular cells via stimulation of insulin-like growth factor-1 receptors and their signaling pathway. Insulin also causes activation of the vascular renin-angiotensin system in both vascular smooth muscle cells and endothelial cells. Insulin-activated tissue renin-angiotensin system leads to increased cell growth and contributes to the cause of atherosclerosis. The fact that agents that inhibit the renin-angiotensin system also block insulin-mediated renin-angiotensin system expression and cell growth reinforces the potential implication of a vascular insulin-renin-angiotensin system pathway. Finally, novel substances such as the adipokines, factors produced from fat cells, reveal new risk factors in the metabolic syndrome and offer further evidence for a link between insulin resistance and accelerated atherosclerosis.
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PMID:Vascular signaling pathways in the metabolic syndrome. 1188 65

Obesity has recently been linked to mortality from the majority of cancers. The insulin/insulin-like growth factor (IGF) system may partly explain this effect. The metabolic syndrome, associated with hyperinsulinemia, may modulate this effect. Recent evidence supports the role of insulin and IGF-1 as important growth factors, acting through the tyrosine kinase growth factor cascade in enhancing tumor cell proliferation. In addition, the metabolic syndrome associated with a chronic inflammatory state and accompanying cytokine abnormalities may also contribute to tumor progression. Growing links between insulin and the etiology as well as prognosis in colon, prostate, pancreatic, and, particularly, breast cancer are reviewed. Of particular concern is the evidence that elevated IGF-1 may interfere with cancer therapy, adversely affecting prognosis. The role of insulin is of concern because of the increasing levels of obesity and the associated metabolic syndrome. Weight gain, through typical Western diet; limited levels of activity; and, more recently, stress-related changes in neuroendocrine function may lead to insulin resistance and hyperinsulinemia. The opportunity for a multidisciplinary approach involving nutrition, exercise, and stress reduction in an integrative setting may be crucial to limiting the insulin-resistant state and improving cancer outcomes.
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PMID:Insulin and cancer. 1471 23

Metabolic syndrome was initially described as an aggregation of risk factors for the development of coronary artery disease with insulin resistance and compensatory hyperinsulinemia as the underlying factor. In an earlier review, we suggested that hyperinsulinemia may also lead to prostate cancer (PCa), the most common male cancer in industrialized nations. Furthermore, we suggested that diet and exercise, known to be important in the development of insulin resistance, may also be important in the development of PCa. When we placed men from the United States on a low-fat diet and/or exercise program, serum levels of insulin, free testosterone, estradiol and insulin-like growth factor (IGF)-1 were reduced while sex hormone-binding globulin (SHBG) and insulin-like growth factor binding protein (IGFBP)-1 were elevated. These in vivo serum changes directly impacted on androgen-dependent prostate cancer cell lines in vitro to reduce cell growth and induce apoptosis. The reduction in serum IGF-1 and increase in IGFBP-1 with diet and exercise appear to be the most significant, as these changes lead to an increase in tumor cell p53 protein and its down-stream effector p21, which are responsible for the reduction in cell growth and induced apoptosis. Preliminary results from a clinical study with men on "watchful waiting" indicate that the observed in vitro effects of diet and exercise on prostate cancer cell growth also occur in vivo.
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PMID:Preclinical models relevant to diet, exercise, and cancer risk. 1564 82

There are only a few data on the relationship of insulin-like growth factor-1 (IGF-1), implicated in glucose homeostasis, and C-reactive protein (CRP), a measure of subclinical systemic inflammation, in patients with the metabolic syndrome (MetS). The authors investigated, in a cross-sectional design, the correlation between total IGF-1 and CRP in 170 subjects. Among them 123 had the MetS (National Cholesterol Program ATP III definition) and 47 did not, and 136 had type 2 diabetes mellitus (DM) and 34 did not. Anthropometric variables, clinical characteristics, as well as laboratory measurements, including total IGF-1 and CRP, were recorded. CRP levels showed a significant negative correlation with total IGF-1 concentrations, both in the whole study population (r = -0.252, p = 0.001) and the MetS group (r = -0.203, p = 0.025), regardless of the presence of DM. This correlation remained significant after adjusting for age, gender, smoking status, and waist circumference (r = -0.18, p = 0.05). Both low IGF-1 and high CRP levels had an almost linear relationship with the number of MetS components (p = 0.029 and p = 0.020, respectively), suggesting a close relationship of both variables with the cardiovascular disease (CVD) risk involved. The correlation between high CRP and low total IGF-1 might indicate that an increase in CRP levels may well be a key factor for the reduction in IGF-1 concentrations. Both factors are related to an increase in risk for MetS and CVD and this finding might have clinical implications in preventing or treating MetS, DM, and CVD. Given the cross-sectional design of the study, this finding should be confirmed by larger prospective and, it is hoped, interventional studies.
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PMID:Total serum insulin-like growth factor-1 and C-reactive protein in metabolic syndrome with or without diabetes. 1670 90

Most of the basic components of the metabolic syndrome, namely type 2 diabetes mellitus, hypertension, obesity, or low high-density lipoprotein cholesterol levels, apart from being major risk factors for cardiovascular disease have been also associated with an increased risk of chronic kidney disease. However, several epidemiologic studies conducted over the past years suggest that the central component of the syndrome, insulin resistance, as well as compensatory hyperinsulinemia are independently associated with an increased prevalence of chronic kidney disease. In addition, background studies support the existence of several pathways linking insulin resistance and hyperinsulinemia with kidney damage. Insulin per se promotes the proliferation of renal cells and stimulates the production of other important growth factors such as insulin-like growth factor-1 and transforming growth factor beta. Insulin also upregulates the expression of angiotensin II type 1 receptor in mesangial cells, thus enhancing the deleterious effects of angiotensin II in the kidney, and stimulates production and renal action of endothelin-1. Moreover, insulin resistance and hyperinsulinemia are associated with decreased endothelial production of nitric oxide and increased oxidative stress which have been also implicated in the progression of diabetic nephropathy. This review analyzes the above and other potential mechanisms, through which insulin resistance and hyperinsulinemia can contribute to renal injury.
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PMID:Insulin resistance, hyperinsulinemia, and renal injury: mechanisms and implications. 1673 48

Estrogen deficiency may be partly responsible for the metabolic syndrome and the condition may be reversible with hormone replacement therapy. However, after the heart and estrogen/progestin replacement study and the women's health initiative study the prospect of HRT on CVD has changed dramatically. As the pituitary and the liver are targets for estrogen action we assessed the effect of ovariectomy (OVX) and long-term (3 months) estradiol (E2) treatment by means of subcutaneously (s.c.) implanted silastic capsules on pituitary and liver function in young and middle-aged female rats. Our results demonstrate that triglyceride serum levels increased, whereas insulin-like growth factor-1 (IGF-1), high density lipoprotein cholesterol (HDL), and glucose levels decreased during the transition from young to middle-age. E2 treatment increased dose-independently growth hormone (GH) secretion. IGF-1 levels were increased upon OVX in middle-aged rats and the high dose of E2 decreased IGF-1 concentrations in both age groups. Cholesterol concentrations increased after OVX and were attenuated by E2 administration in middle-aged rats. Both, low density lipoprotein cholesterol (LDL) and HDL levels raised after castration and both parameters decreased in response to E2 in young and middle-aged rats. Glucose serum concentrations decreased after E2 treatment in all animals. Taken together, our results clearly demonstrate that the pituitary and the liver metabolism of middle-aged rats remain susceptible to the influence of OVX and E2 treatment.
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PMID:Chronic treatment with physiological doses of estradiol affects the GH-IGF-1 axis and fat metabolism in young and middle-aged ovariectomized rats. 1680 12

Metabolic syndrome is associated with dyslipidemia, which is thought to contribute in part to the development of chronic kidney disease (CKD). This review discusses the factors that regulate intracellular handling of lipids and their relationship to disordered mesangial cell function. Specific attention is paid to those factors such as fatty acid translocase/scavenger receptor BII, proliferator-activated receptor delta, insulin-like growth factor-1, inflammation and hypertriglyceridemia that are altered in the metabolic syndrome. CKD also causes an increase in triglycerides and a decrease in high-density lipoprotein that mimic the lipid abnormalities of metabolic syndrome, which accelerate the progression of CKD and increase the risk for cardiovascular mortality. There is a special emphasis on foam cells in the kidney and lipid-mediated changes in intrinsic kidney cells that lead to glomerulosclerosis and interstitial fibrosis. Correlates to whole animal and humans studies are included.
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PMID:Lipid metabolism and renal disease. 1692 36

Many factors are involved in infants' health; one of the most important of them may be the kind of early feeding. Recent evidences suggest that breastfeeding, in addition to its well-established beneficial effects during lactation period, provides also beneficial long-term effects, like the protection against infectious and immune-related diseases, a better cognitive development, a decreased risk of metabolic syndrome and of obesity. It has been reported that the early feeding mode affects growth and body composition and it could be considered a critical factor for metabolic development. Human milk is a source of different nutrients and bioactive factors, especially hormones and growth factors like leptin, ghrelin, insulin, insulin-like growth factor (IGF-I) playing a role in food intake regulation, metabolism and body composition. In particular breast milk leptin may provide a physiological explanation for a number of advantages seen in reaching proper growth and energy balance in breast-fed infants compared with formula fed ones. Etiopathogenesis and therapeutic approach in common minor gastrointestinal diseases in infants are important subject of study for pediatricians. Colic, constipation and regurgitation can be considered feeding problems and they might benefit from dietary treatment. Regarding infantile colic, dietary modifications seem to be more suitable than pharmacological treatment in resolving symptoms; also prebiotics and probiotics are useful for this aim. The occurence of constipation is related to the kind of feeding and it is lower in breastfed infants. Moreover formulas with probiotics and beta-palmitic acid could promote a regression of symptoms. A dietary approach may be useful also in regurgitation. Anyway we have to remember that breastfeeding require a supplementation of vitamin D and K for some months and a correct weaning program is needed from the 5th-6th months of life to prevent iron deficiency.
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PMID:[Breast milk: biological constituents for health and well-being in infancy]. 1726 42

Metabolic syndrome is a cluster of metabolic abnormalities consisting essentially of obesity, especially abdominal obesity. Metabolic syndrome has been highlighted as a risk factor for cardiovascular and other chronic diseases. Obesity has been implicated in various gastrointestinal diseases such as gastroesophageal reflux diseases and colorectal cancer. Recently, abdominal obesity has been shown to be more important than obesity as expressed by an elevated body mass index as a causative factor for the development of these diseases. In addition to the mechanical effects of obesity, such as an increase in intra-abdominal pressure from large amounts of adipose tissue, substances that adipose tissues secrete, such as tumor necrosis factor-alpha, interleukin-6, leptin, and insulin-like growth factor-1, have been proposed to be pathogenic links to these diseases. In this review, we discuss the association of metabolic syndrome or the individual components of metabolic syndrome, focusing on obesity and abdominal obesity, with gastrointestinal diseases.
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PMID:Metabolic syndrome and gastrointestinal diseases. 1746 54


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