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

Trends of prevalence and incidence rates of non-insulin-dependent diabetes mellitus (non-insulin-treated diabetes mellitus) were assessed in the population of the GDR based upon the National Diabetes Register and the Official Statistical Year Book as sources for the calculations. Within the 25-year follow-up period 1960-1984 the prevalence rose from 4.39%; to 31.95%; the incidence rate from 1.04%; to 3.57%. Age-dependence of the specific rates is characterized by their continuous rise above the age of 30 years reaching the peak prevalence of 146.6%; in 75- to 80-year-olds, that of 14.1%, for the incidence in people aged 70 to 75 years. A significant male preponderance was confirmed between the ages of 30 and 50 years, a significant overwhelming of female NIDDM in the age groups 60 to 90 years. Based on demonstrated correlations between the changes of living standard parameters and the epidemiological trend of NIDDM the conclusion is drawn that overnutrition and reduced muscular activity mainly account for the rise of diabetes morbidity in the population of the GDR.
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PMID:Prevalence and incidence trends of non-insulin-dependent diabetes mellitus (NIDDM) in the population of the GDR. 350 32

An investigation was undertaken in Northeast Thailand, a country undergoing rapid health transition, to find out whether there is a likelihood that the nutritional and lipid pattern of an adult population in Northeast Thailand is related to coronary heart disease in the same way as in western countries. In a cross-sectional study, the body mass index (BMI) and the waist-hip ratio as well as the important plasma lipids were determined. The nutritional status and the lipid profile of the predominantly middle-aged population is characterised by a generally favourable nutritional status and lipid concentrations, where the distribution, indicated by the medians, of the relevant variables over the total population is concerned. A rather high proportion of individuals was found to be overnourished and to have high triglyceride levels. Individuals with high triglyceride levels run a risk of developing coronary heart disease only when the LDL-HDL fraction is above 5. Only 3% of the total population investigated had a LDL-HDL ratio above that value. Since hypertriglyceridaemia is also linked to the insulin-resistant syndrome, it is concluded that, if the mortality of coronary heart disease increases in future, then this must be accounted probably more to the after-effects of the insulin-resistant syndrome than to the direct effect of an atherogenic lipid pattern. This view is supported by a high prevalence of impaired glucose tolerance (IGT) and non-insulin dependent diabetes mellitus (NIDDM) in the population under survey. Preventive measures in the area should concentrate among others on reducing overnutrition, especially among women, and increasing physical activity and screening for NIDDM.
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PMID:Nutritional status and serum lipids of a rural population in Northeast Thailand--an example of health transition. 963 51

Body weight and the prevalence of obesity are rising so rapidly in many countries that the World Health Organization has recognized that there is a "global epidemic of obesity." The prevalence of type 2 diabetes is rising in parallel. In view of its associated cardiovascular complications, we are facing a severe public health problem. Both obesity and type 2 diabetes have a combined genetic and environmental background, but the epidemic must be due to major changes in the environment. By definition, obesity is a result of a positive energy balance, which usually amounts to a tiny proportion of the total energy turnover. Energy intake, energy expenditure, and energy accumulation (as fat) may all be primarily disturbed. There is a great, and still insufficiently understood, variation in prevalence of obesity and in the rate of change of the prevalence. The prevailing contention is that the epidemic is due to the changes in the society--the so-called modernization--leading to overnutrition and a sedentary life. These factors are likely contributors, but it has been difficult to provide consistent evidence for their effects. In Denmark, a steep rise has taken place in the prevalence of obesity among schoolboys and young men in two phases linked to the birth cohorts of the 1940s and of the mid-1960s and later. This rise suggests that environmental influences operating early in life are involved. In conclusion, a global obesity epidemic is developing, but the causes of the epidemic are not yet clear and more research is needed to establish the grounds for prevention.
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PMID:The changing lifestyle in the world. Body weight and what else? 1086 Jan 83

When the fetus growth in an unfavorable intrauterine environment, this process has implications in the adult life, that predisposes to suffer metabolic abnormalities as obesity, hypertension and non-insulin dependent diabetes mellitus. The unfavorable intrauterine environment includes the pregnancy with diabetes mellitus, pregnancy with gestational diabetes, and pregnancy with maternal undernutrition. Multiple epidemiological studies developed in North America and Europe appear to broadly confirm the association of the low birth weight in babies borne at term, with the glucose metabolism impairments in the adult life. An implication of metabolic impairments on high birth weight for the gestational age has been founded. This alteration could start when there are changes in nutritional habits in migrate populations, having number and function of the pancreatic islets altered, maybe because during fetal life they were faced to blood fluid decreased, and nutrients also decrease as well as the differentiation of cells was modified, as an important intent for fetal survival. The prevalence of type 2 diabetes has been reported in 13 to 25% for low birth weight. On the other hand, maternal hyperglycemia leads to beta-cell hyperplasia in the fetus, by a constant stimulus over the insulin production which stimulates the use of glucose as nutrients, leading to the increase in fetal weight and determining genetic changes. In overnutrition conditions, the prevalence of type 2 diabetes has been reported of 8 to 18%. Growth of tissues has critical periods at different times and intrauterine environment can be one mechanism for may permanently changes in pancreas structure and hormonal secretion patterns. Thus, the hypothesis that autoprotective fetal changes during the intrauterine life occur, took place, specially during the critical period of development, leaves to permanent changes called "programmed changes", including an endocrine disturbance of pancreatic functions, appearing in adult life. Further molecular studies of pancreatic islets are necessary in order to determine the mechanisms for lifelong changes and insulin metabolism due to intrauterine growth.
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PMID:[Fetal weight at weight as predisposing risk factor for type 2 diabetes in adulthood]. 1181 27

I review evidence that leptin is a liporegulatory hormone that controls lipid homeostasis in nonadipose tissues during periods of overnutrition. When adipocytes store excess calories as triacylglycerol (TG), leptin secretion rises so as to prevent accumulation of lipids in nonadipose tissues, which are not adapted for TG storage. Whenever leptin action is lacking, whether through leptin deficiency or leptin resistance, overnutrition causes disease of nonadipose tissues with generalized steatosis, lipotoxicity, and lipoapoptosis. Examples of such disorders of liporegulation include generalized lipodystrophies, mutations of leptin and leptin receptor genes, and diet-induced obesity. Lipotoxicity of pancreatic beta-cells, myocardium, and skeletal muscle leads, respectively, to type 2 diabetes, cardiomyopathy, and insulin resistance. In humans this constellation of abnormalities is referred to as the metabolic syndrome, a major health problem in the United States. When lipids overaccumulate in nonadipose tissues during overnutrition, fatty acids enter deleterious pathways such as ceramide production, which, through increased nitric oxide formation, causes apoptosis of lipid-laden cells, such as beta-cells and cardiomyocytes. Lipoapoptosis can be prevented by caloric restriction, by thiazolidinedione treatment, and by administration of nitric oxide blockers. There is now substantial evidence that complications of human obesity may reflect lipotoxicity similar to that described in rodents.
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PMID:Lipotoxic diseases. 1181 77

The underlying determinants of cardiovascular risk are governed by both genetic and lifestyle factors. One of the major adverse outcomes of unhealthy lifestyles is obesity, the genesis of which begins in childhood. Obesity, an important risk factor for atherosclerotic cardiovascular disease, type 2 diabetes, and hypertension, persists (tracks) strongly from adolescent years to adulthood. Secular trends toward increased obesity in the past 25 years have occurred in children and adults alike. Of interest, baseline adiposity precedes hyperinsulinemia in all age groups, independently of race, sex, and baseline insulin levels. Adiposity is an independent predictor of the risk of developing the cluster of risk variables of the metabolic syndrome X, beginning in childhood. Exposure to a multiple risk factor burden over time enhances the development of coronary atherosclerosis and hypertensive cardiovascular disease. In fact, autopsy studies in youths have shown that the extent of fibrotic atherosclerotic plaques in coronary arteries, measured antemortem, increases markedly with the presence of syndrome X risk variables. Further, in overweight children, insulin levels are associated with left ventricular mass. In young people, overnutrition, coupled with physical inactivity, leads to weight gain. Since obesity, unhealthy dietary habits, and a sedentary lifestyle are interrelated and modifiable, prevention and intervention must begin in early life. (c)2001 CHF, Inc.
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PMID:Emergence of obesity and cardiovascular risk for coronary artery disease: the Bogalusa Heart Study. 1182 87

During the last five decades the metabolic syndrome has turned into an epidemic in countries with overnutrition and low levels of physical activity. About 15% of the population aged 40-75 in these countries exhibit exhibit the 'metabolic syndrome' cluster diseases. We define the metabolic syndrome as a cluster of diseases with at least three of the following components diagnosed in any one subject: ITG/type 2 diabetes, android obesity, dyslipidemia, hypertension, hyperuricemia, albuminuria and atherosclerosis. Insulin resistance was found in more than 80% of both the clinical type 2 diabetics and the subjects with IGT in the RIAD study. Intra-abdominal obesity and lipotoxicity are other important causes. Today the metabolic syndrome is--and for the near future will continue to be--the most important source of new diabetics, as well as a major cause of coronary heart disease.
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PMID:[The metabolic syndrome and its epidemiologic dimensions in historical perspective]. 1201 62

High concentrations of glucose induce insulin resistance and impair insulin secretion in a manner that mirrors type 2 diabetes, a phenomenon known as glucose toxicity. High concentrations of hexosamines mimic these effects, leading to the hypothesis that cells use hexosamine flux as a glucose- and satiety-sensing pathway. Overexpression of the rate-limiting enzyme for hexosamine synthesis (glutamine:fructose-6-phosphate amidotransferase, GFA) in muscle and fat results in insulin resistance and hyperleptinemia. GFA overexpression targeted to liver results in hyperlipidemia and to the beta cell in increased insulin secretion. Thus, excess hexosamine flux leads to a coordinated response whereby fuel is shunted toward long-term storage, mirroring the "thrifty phenotype". The results suggest a mechanism by which chronic overnutrition leads to the phenotype of type 2 diabetes.
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PMID:Transgenic mice overexpressing the rate-limiting enzyme for hexosamine synthesis in skeletal muscle or adipose tissue exhibit total body insulin resistance. 1207 40

Beta-cells possess inherent mechanisms to adapt to overnutrition and the prevailing concentrations of glucose, fatty acids, and other fuels to maintain glucose homeostasis. However, this is balanced by potentially harmful actions of the same nutrients. Both glucose and fatty acids may cause good/adaptive or evil/toxic actions on the beta-cell, depending on their concentrations and the time during which they are elevated. Chronic high glucose dramatically influences beta-cell lipid metabolism via substrate availability, changes in the activity and expression of enzymes of glucose and lipid metabolism, and modifications in the expression level of key transcription factors. We discuss here the emerging view that beta-cell "glucotoxicity" is in part indirectly caused by "lipotoxicity," and that beta-cell abnormalities will become particularly apparent when both glucose and circulating fatty acids are high. We support the concept that elevated glucose and fatty acids synergize in causing toxicity in islets and other organs, a process that may be instrumental in the pleiotropic defects associated with the metabolic syndrome and type 1 and type 2 diabetes. The mechanisms by which hyperglycemia and hyperlipidemia alter insulin secretion are discussed and a model of beta-cell "glucolipotoxicity" that implicates alterations in beta-cell malonyl-CoA concentrations; peroxisome proliferator-activated receptor-alpha and -gamma and sterol regulatory element binding protein-1c expression; and lipid partitioning is proposed.
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PMID:Malonyl-CoA signaling, lipid partitioning, and glucolipotoxicity: role in beta-cell adaptation and failure in the etiology of diabetes. 1247 83

The ability to regulate energy balance at both the cellular and whole body level is an essential process of life. As western society has shifted to a higher caloric diet and more sedentary lifestyle, the incidence of type 2 diabetes (non-insulin-dependent diabetes mellitus) has increased to epidemic proportions. Thus, type 2 diabetes has been described as a disease of 'chronic overnutrition'. There are abundant data to support the relationship between nutrient availability and insulin action. However, there have been multiple hypotheses and debates as to the mechanism by which nutrient availability modulates insulin signaling and how excess nutrients lead to insulin resistance. One well-established pathway for nutrient sensing is the hexosamine biosynthetic pathway (HSP), which produces the acetylated aminosugar nucleotide uridine 5'-diphospho-N-acetylglucosamine (UDP-Glc-NAc) as its end product. Since UDP-GlcNAc is the donor substrate for modification of nucleocytoplasmic proteins at serine and threonine residues with N-acetylglucosamine (O-GlcNAc), the possibility of this posttranslational modification serving as the nutrient sensor has been proposed. We have recently directly tested this model in adipocytes by examining the effect of elevated levels of O-GlcNAc on insulin-stimulated glucose uptake. In this review, we summarize the existing work that implicates the HSP and O-GlcNAc modification as nutrient sensors and regulators of insulin signaling.
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PMID:A role for N-acetylglucosamine as a nutrient sensor and mediator of insulin resistance. 1267 87


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