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Query: UMLS:C0011860 (type 2 diabetes)
 57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have reviewed whether the complications of obesity can be attributed to low levels of physical activity and fitness, or if fatness per se has adverse effects on health. In both observational and interventional studies, fatness and inactivity seem to be independent risk factors. Abdominal obesity is a predictor of cardiovascular disease, which is independent of low fitness level, and obesity affects other risk factors adversely than inactivity does. However, physical activity does reduce the risk of type 2 diabetes and heart disease. It is concluded that both inactivity and obesity have an adverse effect on health.
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PMID:[The importance of physical activity and fitness in avoiding the complications of obesity]. 1640 37

Most patients with type 2 diabetes die from heart disease. Screening for the presence of myocardial ischemia is of clinical importance in the management of this population. The pain response to ischemia can be either absent or blunted in diabetes, resulting in the absence of symptoms or an atypical presentation. Exercise electrocardiogram (ECG) should be the initial test in men who are able to exercise and have a normal resting ECG. Stress cardiac imaging should be the initial test in diabetic men with an abnormal resting ECG or who are not able to exercise. More widespread use of cardiac imaging is probably justified in diabetic women and patients with suspected coronary artery disease. Official guidelines for appropriate and cost-effective cardiac investigation should help physicians manage diabetic patients.
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PMID:Cardiac investigation in patients with diabetes. 1648 59

The Metabolic syndrome is a widely prevalent and multi-factorial disorder. The syndrome has been given several names, including- the metabolic syndrome, the insulin resistance syndrome, the plurimetabolic syndrome, and the deadly quartet. With the formulation of NCEP/ATP III guidelines, some uniformity and standardization has occurred in the definition of metabolic syndrome and has been very useful for epidemiological purposes. The mechanisms underlying the metabolic syndrome are not fully known; however resistance to insulin stimulated glucose uptake seems to modify biochemical responses in a way that predisposes to metabolic risk factors. The clinical relevance of the metabolic syndrome is related to its role in the development of cardiovascular disease. Management of the metabolic syndrome involves patient-education and intervention at various levels. Weight reduction is one of the main stays of treatment. In this article we comprehensively discuss this syndrome- the epidemiology, pathogenesis, clinical relevance and management. The need to do a comprehensive review of this particular syndrome has arisen in view of the ever increasing incidence of this entity. Soon, metabolic syndrome will overtake cigarette smoking as the number one risk factor for heart disease among the US population. Hardly any issue of any primary care medical journal can be opened without encountering an article on type 2 diabetes, dyslipidemia or hypertension. It is rare to see type 2 diabetes, dyslipidemia, obesity or hypertension in isolation. Insulin resistance and resulting hyperinsulinemia have been implicated in the development of glucose intolerance (and progression to type 2 diabetes), hypertriglyceridemia, hypertension, polycystic ovary syndrome, hypercoagulability and vascular inflammation, as well as the eventual development of atherosclerotic cardiovascular disease manifested as myocardial infarction, stroke and myriad end organ diseases. Conversely, treatment and consequent improvement of insulin resistance have been shown to result in better outcomes in virtually all of these conditions.
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PMID:Metabolic syndrome. 1650 79

Researchers are only gradually becoming aware of the gravity of the risk that overweight and obesity pose for children's health. In this article Stephen Daniels documents the heavy toll that the obesity epidemic is taking on the health of the nation's children. He discusses both the immediate risks associated with childhood obesity and the longer-term risk that obese children and adolescents will become obese adults and suffer other health problems as a result. Daniels notes that many obesity-related health conditions once thought applicable only to adults are now being seen in children and with increasing frequency. Examples include high blood pressure, early symptoms of hardening of the arteries, type 2 diabetes, nonalcoholic fatty liver disease, polycystic ovary disorder, and disordered breathing during sleep. He systematically surveys the body's systems, showing how obesity in adulthood can damage each and how childhood obesity exacerbates the damage. He explains that obesity can harm the cardiovascular system and that being overweight during childhood can accelerate the development of heart disease. The processes that lead to a heart attack or stroke start in childhood and often take decades to progress to the point of overt disease. Obesity in childhood, adolescence, and young adulthood may accelerate these processes. Daniels shows how much the same generalization applies to other obesity-related disorders-metabolic, digestive, respiratory, skeletal, and psychosocial-that are appearing in children either for the first time or with greater severity or prevalence. Daniels notes that the possibility has even been raised that the increasing prevalence and severity of childhood obesity may reverse the modern era's steady increase in life expectancy, with today's youth on average living less healthy and ultimately shorter lives than their parents-the first such reversal in lifespan in modern history. Such a possibility, he concludes, makes obesity in children an issue of utmost public health concern.
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PMID:The consequences of childhood overweight and obesity. 1653 58

Obesity is a major risk factor for heart disease. In the face of obesity's growing prevalence, it is important for physicians to be aware of emerging research of novel mechanisms through which adiposity adversely affects the heart. Conventional wisdom suggests that either hemodynamic (that is, increased cardiac output and hypertension) or metabolic (that is, dyslipidemic) derangements associated with obesity may predispose individuals to coronary artery disease and heart failure. The purpose of this review is to highlight a novel mechanism for heart disease in obesity whereby excessive lipid accumulation within the myocardium is directly cardiotoxic and causes left ventricular remodeling and dilated cardiomyopathy. Studies in animal models of obesity reveal that intracellular accumulation of triglyceride renders organs dysfunctional, which leads to several well-recognized clinical syndromes related to obesity (including type 2 diabetes). In these rodent models, excessive lipid accumulation in the myocardium causes left ventricular hypertrophy and nonischemic, dilated cardiomyopathy. Novel magnetic resonance spectroscopy techniques are now available to quantify intracellular lipid content in the myocardium and various other human tissues, which has made it possible to translate these studies into a clinical setting. By using this technology, we have recently begun to study the role of myocardial steatosis in the development of obesity-specific cardiomyopathy in humans. Recent studies in healthy individuals and patients with heart failure reveal that myocardial lipid content increases with the degree of adiposity and may contribute to the adverse structural and functional cardiac adaptations seen in obese persons. These studies parallel the observations in obese animals and provide evidence that myocardial lipid content may be a biomarker and putative therapeutic target for cardiac disease in obese patients.
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PMID:Adiposity of the heart, revisited. 1701 81

Obesity is a heritable trait and a risk factor for many common diseases such as type 2 diabetes, heart disease, and hypertension. We used a dense whole-genome scan of DNA samples from the Framingham Heart Study participants to identify a common genetic variant near the INSIG2 gene associated with obesity. We have replicated the finding in four separate samples composed of individuals of Western European ancestry, African Americans, and children. The obesity-predisposing genotype is present in 10% of individuals. Our study suggests that common genetic polymorphisms are important determinants of obesity.
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PMID:A common genetic variant is associated with adult and childhood obesity. 1721 10

Fetal programming is gaining momentum as a highly documented phenomenon which links poor early growth to adult disease. It is backed up by large cohorts in epidemiological studies worldwide and has been tested in various animal models. The root causes of programming link closely with maternal condition during pregnancy, and therefore the fetal environment. Suboptimal fetal environments due to poor or inadequate nutrition, infection, anemia, hypertension, inflammation, gestational diabetes or hypoxia in the mother expose the fetus to hormonal, growth factor, cytokine or adipokine cues. These in turn act to alter metabolic, immune system, vascular, hemodynamics, renal, growth and mitochondrial parameters respectively and most evidently in the later stages of life where they impact on the individual as poor glucose homeostasis, insulin resistance, type 2 diabetes, hypertension, cardiovascular disease, obesity and heart disease. These events are compounded by over-nutrition or lifestyle choices which are in conflict with the programming of the fetus. We and others have utilised various species to test the early life programming hypothesis and to identify key molecular mechanisms. With parallel studies of human cohorts, these molecular markers can be validated as realistic targets for intervention.
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PMID:Mechanisms by which poor early growth programs type-2 diabetes, obesity and the metabolic syndrome. 1678 39

The metabolic syndrome has been referred to as a clustering of cardiovascular risk factors, including abdominal obesity, atherogenic dyslipidemia, increased blood pressure, insulin resistance, proinflammatory state, and a prothrombotic state. The metabolic syndrome has become one of the leading clinical issues discussed by physicians and the media, leading to increased public awareness to this potentially catastrophic multiplex risk factor for cardiovascular disease. With increasing prevalence in the United States, the metabolic syndrome has been equated to cigarette smoking as a contributing factor to premature cardiovascular heart disease and one of the underlying causes of type 2 diabetes. The identification and modification of the root causes, overweight/obesity, physical inactivity, and the closely associated condition, insulin resistance, needs to be one of the initial strategies that are addressed by the clinician.
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PMID:What is the metabolic syndrome? Prediabetes and cardiovascular risk. 1682 82

Only 13% of those 65 years and older engage in vigorous physical activity 3 or more days a week and obesity rates are increasing by 45% in adults over the age of 60. Physical activity helps prevent chronic disease and improves quality of life, yet few adults of any age are active. One exception is master athletes who participate in competitive sports during the middle and later years. The aerobic fitness of master athletes, as measured by maximal oxygen consumption, shows some decline, but not nearly as much as in sedentary controls. Master athletes have lipid profiles similar to those of young adults, which decreases their risk of heart disease. Master athletes also have better glucose tolerance and lower waist-to-hip ratios than sedentary adults, decreasing their risk for metabolic syndrome and type 2 diabetes. In the few dietary studies that have been conducted, master athletes consume more food energy while maintaining lower body weights than sedentary adults. Learning what motivates master athletes to stay highly active may help health professionals develop strategies to encourage exercise in the sedentary population of older adults.
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PMID:What can we learn about diet and physical activity from master athletes? 1682 17

Obesity endangers the lives of millions of people worldwide, through comorbidities such as heart disease, cancers, type 2 diabetes, stroke, arthritis, and major depression. New approaches to control body weight remain a high priority. Vaccines traditionally have been used to protect against infectious diseases and, more recently, for unconventional targets such as drug addiction. Methodologies that could specifically modulate the bioavailability of an endogenous molecule that regulates energy balance might provide a new foundation for treating obesity. Here we show that active vaccination of mature rats with ghrelin immunoconjugates decreases feed efficiency, relative adiposity, and body weight gain in relation to the immune response elicited against ghrelin in its active, acylated form. Three active vaccines based on the 28-aa residue sequence of ghrelin, a gastric endocrine hormone, were used to immunize adult male Wistar rats (n = 17). Synthetic ghrelin analogs were prepared that spanned residues 1-10 [ghrelin (1-10) Ser-3(butanoyl) hapten, Ghr1], 13-28 [ghrelin (13-28) hapten, Ghr2], and 1-28 [ghrelin(1-28) Ser-3(butanoyl) hapten, Ghr3], and included n-butanoyl esters at Ser-3. Groups immunized with Ghr1 or Ghr3 showed greater and more selective plasma binding capacity for the active, Ser-3-(n-octanoyl) form of ghrelin as compared with Ghr2 or keyhole limpet hemocyanin vaccinated controls. Accordingly, they gained less body weight, with sparing of lean mass and preferential reduction of body fat, consistent with reduced circulating leptin levels. The ratio of brain/serum ghrelin levels was lower in rats with strong anti-ghrelin immune responses. Effects were not attributable to nonspecific inflammatory responses. Vaccination against the endogenous hormone ghrelin can slow weight gain in rats by decreasing feed efficiency.
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PMID:Vaccination against weight gain. 1692 97


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