UMLS:C0028754 - FACTA Search

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Query: UMLS:C0028754 (obesity)
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Hyperglycemia and other metabolic derangements resulting from absolute or functional deficiency of insulin are accompanied by typical signs and symptoms of diabetes. The clinical signs and the findings of hyperglycemia over 200 mg/dl should establish a diagnosis of diabetes mellitus. An oral glucose tolerance test (O-GTT) is rarely necessary for diagnosis of diabetes in a child. A small proportion of children, however, present less severe symptoms, and may require an O-GTT. Approximately 14% of IDDM children were in coma at diagnosis in Tokyo, and 11 onset deaths (0.94%) were observed among the 1172 newly diagnosed IDDM cases in Japan. A significant decline in the onset mortality, however, has been observed in the past 20 years in Japan in association with the improvement of early management of childhood diabetes. The clinical distinction of IDDM from NIDDM is often difficult in diabetic children of Oriental origin without obesity. Japanese IDDM can be divided into two forms, abrupt and slow onset forms, but they may be essentially the same disease. There was no difference in the frequency of being tested positive for circulating ICA between the two groups of the patients. But a difference in the frequency of HLA DR4 and DRW9 was noticed between the two groups. Clinical features of 107 children with NIDDM were studied and about 75% of these cases were obese. All of them can be detected by routine urinalysis for glucose. Diet and exercise therapy in most of the newly diagnosed patients resulted in remission but some of them may require insulin or an oral hypoglycemic agent to get better glycemic control.
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PMID:Initial signs and diagnosis of diabetes--special considerations of Oriental patients. 263 91

Since the 1940s, many Amerindian populations, including some with mixed Amerindian ancestry, have experienced an epidemic of obesity and adult-onset diabetes (NIDDM). Obesity and NIDDM were apparently rare among Amerindian populations prior to that time. Though the evidence is equivocal, obesity and NIDDM seem to be rare today among Athapaskan Amerindians of the North American Arctic, sub-Arctic, and Southwest. It is hypothesized that the Amerindian genotype(s) susceptible to obesity and NIDDM arose from selection favoring "thrifty" genes during the peopling of North America south of the continental glaciers. "Thrifty" genes (Neel: Am. J. Hum. Genet. 14:353-362, 1962) allowed a more efficient food metabolism as hunter-gatherers from an unusually harsh mid-latitude tundra environment (the "ice free" corridor) adapted to more typical mid-latitude environments to the south. The early Paleoindian settlement pattern from Wyoming to Arizona and Texas indicates a relatively brief period of reliance on unpredictable big game resources in lower elevations and smaller game and gathered resources in higher elevations. This unusual "specialist" settlement pattern may have resulted from the early Paleoindian's unfamiliarity with gathered foods and small game in lower elevations. Athapaskan populations evidently moved south from Beringia sometime after the Paleoindian migration when the "ice free" corridor had widened and contained environments and resources more typical of subarctic latitudes. Thus, Athapaskan hunter-gatherers could gradually adapt to the resources of lower latitudes such that "thrifty" genes would not have been as advantageous. The interaction of recently introduced "western" diets and "thrifty" genes have evidently led to today's epidemic of obesity and NIDDM among Amerindians of Paleoindian ancestry.
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PMID:Diabetes, the ice free corridor, and the Paleoindian settlement of North America. 267 32

The importance of genetic factors in the aetiology of NIDDM has been underlined by study of family pedigrees and identical twin pairs. Although in some isolated populations and a tiny minority of Western families inheritance follows an autosomal dominant pattern, a polygenic mode of transmission predominates in Europe and North America. No genetic markers have been identified despite intensive study of the HLA system and gene polymorphisms. Environmental factors appear to play some role, but examination of the evidence for an aetiological effect of the commonly assumed factors, diet and obesity, suggests that they exert no direct effect. However, it is likely that these factors together with physical inactivity could modulate the speed of progression to symptomatic disease. Both beta cell dysfunction and tissue insulin insensitivity are important in producing the syndrome of NIDDM. Insulin insensitivity is present from very early in the time course of the syndrome, but it is clear that the disease cannot develop in the absence of beta cell dysfunction. The recent discovery of islet associated amyloid is exciting as it represents a major step in tracing the pathogenesis of NIDDM backwards towards genetic and non-genetic aetiological influences.
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PMID:Aetiology of non-insulin dependent diabetes. 267 75

NIDDM is the predominant form of diabetes mellitus in all populations, almost exclusively so in some. Its prevalence varies enormously, with particularly high rates in populations whose lifestyle has drastically changed since World War II. Epidemiologic data from the developed countries of Europe and North America are not adequate to determine whether their incidence rates have also increased. Genetic factors are clearly implicated in the etiology of NIDDM, but their location and mode of expression remain to be determined. The two variables most strongly related to the incidence of NIDDM are age and degree of obesity, although there is emerging evidence of an independent association with fat distribution. Whether the nature of the habitual diet and the degree of physical activity influence the incidence of NIDDM remains uncertain and should be further researched. Cardiovascular disease is strongly associated with NIDDM in most populations, but there are between-population differences in the degree of association and the relative excess in the two sexes. There is increasing evidence, in particular for coronary heart disease, that increased risk precedes the onset of hyperglycemia; the implication of this is that NIDDM and atherosclerosis share common antecedents. The specific complications of NIDDM--eye and renal disease--are important causes of morbidity and mortality and for those populations, often relatively poor, in which NIDDM is already or is becoming very common will pose substantial problems in provision of health care.
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PMID:Epidemiology and public health aspects of non-insulin-dependent diabetes mellitus. 268 May 53

Amylin, the major peptide component of the islet amyloid commonly found in the pancreases of patients with type 2 (non-insulin-dependent) diabetes mellitus (NIDDM), is a recently discovered islet polypeptide. This peptide has many structural and functional features suggesting that it is a novel hormone, which may control carbohydrate metabolism in partnership with insulin and other glucoregulatory factors. Amylin is synthesised in, and probably secreted from, the beta-cells of the islets of Langerhans, where it has recently been immunolocalised to secretory granules. DNA cloning studies indicate that in the human and the rat, amylin is generated from a precursor, preproamylin, which displays a typical signal peptide followed by a small prohormone-like sequence containing the amylin sequence. The presence of the signal peptide suggests that amylin is secreted and plays a physiological role. Amylin is probably generated by proteolytic processing similar to that for proinsulin and other islet prohormones. The human amylin gene encodes the complete polypeptide precursor in two exons which are separated by an intron of approx. 5 kb, and is located on chromosome 12. Amylin is a potent modulator of glycogen synthesis and glucose uptake in skeletal muscle, and is capable of inducing an insulin-resistant state in this tissue in vitro, and perhaps also in the liver in vivo. In normal metabolism, amylin could act in concert with insulin as a signal for the body to switch the site of carbohydrate disposal from glycogen to longer-term stores in adipose tissue, by making skeletal muscle relatively insulin-resistant, whilst at the same time leaving rates of insulin-stimulated carbohydrate metabolism in adipose tissue unaltered. Several lines of evidence now implicate elevated amylin levels in the pathogenic mechanisms underlying NIDDM, and suggest to us that the obesity which frequently accompanies this syndrome is a result of, rather than a risk factor for, NIDDM. Following the beta-cell destruction which occurs in type 1 (insulin-dependent) diabetes mellitus (IDDM), it is probable that amylin secretion disappears in addition to that of insulin. As patients with insulin-treated IDDM frequently experience problems with hypoglycaemia, and as amylin acts to modulate the action of insulin in various tissues, it is possible that amylin deficiency may contribute to morbidity in insulin-treated IDDM, perhaps through the loss of a natural damping mechanism which guards against hypoglycaemia under conditions of normal physiology.
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PMID:Amylin and the amylin gene: structure, function and relationship to islet amyloid and to diabetes mellitus. 269 Sep 58

Nineteen diabetics aged 9 to 18 years with the MODY type were investigated, incl. their families, by the oGTT. Diabetes in the parents was nine times and in siblings four times more frequent than in families of adolescents with IDDM. In parents the manifest form predominated, in siblings PGT. Vertical transmission of diabetes in three consecutive generations was found only in the MODY type (in 35%). Diabetes with the MODY type and their diabetic siblings did not differ significantly as to their mild glucose intolerance (blood sugar level up to 13 mmol/l), and their mild diabetic phenotypes did not differ either. Similarly diabetics with IDDM and their diabetic siblings did not differ substantially as to their severe glucose intolerance (blood sugar level up to 21 mmol/l), and their severe diabetic phenotypes did not differ either. IRI levels revealed five times a hyperinsulinaemic and three times a normal insulinaemic response. Obese diabetics were treated with a reducing diet and physical activity. To non-obese diabetics, if the above procedure was not sufficiently successful, sulphonylurea preparation were also administered. During check-up examinations fasting values and values three hours after a meal lower than 6.1 mmol/l were required. In the course of a four- to ten-year follow up it did not change. Existence of the MODY type already macroangiopathic complications developed; in one diabetic the glucose tolerance improved, in the remainder it did not change. Existence of the MODY type already in adolescents justifies early detection in families with a cumulated incidence of NIDDM and prophylactic procedures ensuring euglycaemia in confirmed diabetics.
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PMID:[MODY type diabetes mellitus in children and adolescents]. 275 88

Insulin clamp studies were carried out on 13 non-diabetics and 12 non-insulin-dependent diabetics (NIDDM). Based upon the body mass index (BMI), they were further divided into obese (BMI greater than or equal to 27 kg/m2) and nonbese groups (BMI less than 27 kg/m2). All received euglycemic insulin clamp study (Humulin-S 40mU/m2/min). Thermoregulated venous samplings were done every five minutes for measurements of plasma glucose (PG) and immunoreactive insulin (IRI). Steady state plasma glucose (SSPG) was obtained 20-80 minutes and kept for 100 more minutes. The data of final 40 minutes of clamp were used for analysis. Variations in SSPG and metabolic clearance rate of glucose (MCRG) instead of glucose infusion rate (M) value were used to assess the insulin sensitivity. The results showed that insulin resistance was noted in obese non-diabetic and diabetic subjects as well as in non-obese diabetic patients, as evidenced by higher basal IRI and lower MCRG than non-obese normal controls. Correlation analysis revealed that there was no correlation between the reduction of MCRG and the BMI in either non-diabetic or diabetic patients. There was a strong negative correlation between MCRG and the ambient fasting plasma glucose in the diabetic group, whereas this correlation was not found in the non-diabetic group. In conclusion, obesity with or without diabetes did have remarkable insulin resistance. In non-diabetic obese subjects the insulin resistance did not go up as the BMI increased further. In diabetic patients, both obesity and hyperglycemia contributed significantly insulin resistance.
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PMID:Insulin resistance in obesity and noninsulin dependent diabetes mellitus. 276 59

In 107 patients with non-insulin dependent diabetes(NIDDM), plasma growth hormone(GH) responses during standard arginine test (0.5 g/kg of body weight) were studied and analyzed in comparison with those in 17 normal subjects. The indices of the responsiveness of GH, peak value of GH, sum of GH values(sigma GH), area of GH curve(integral of GH), sum of GH values above fasting level(sigma delta GH) and area of GH curve above fasting level(integral of delta GH) during the test (2 hr) were calculated. Data were also analyzed with multiple regression analysis using stepwise method for variable selection. Basal level of GH was significantly higher in diabetic patients than in normal subjects (2.1 +/- 1.7 vs. 1.6 +/- 0.5 ng/ml, mean +/- SD, p less than 0.05), and sigma GH and integral of GH were also higher in diabetic patients. There was a significantly positive correlation between fasting plasma glucose(FPG) and basal level of GH (r = 0.24, n = 107, p less than 0.05), and the indices of GH responses except delta GH and GH peak value (r = 0.24 to 0.31, p less than 0.05 to 0.01). Some indices of GH responses (sigma delta GH, sigma GH, integral of delta GH and integral of GH) were significantly higher in the poor control group (patients with FPG above 180 mg/dl, n = 29) of diabetic patients than in the good control group (patients with FPG below 140 mg/dl, n = 59), or in the group with no abnormal findings of retinopathy (n = 46). During the follow-up of retinopathy for 2.5 years on the average, progression of retinopathy was found in 21 out of 107 patients. Significantly higher GH, and GH in the patients with increasing severity of retinopathy were revealed retrospectively compared to the patients without it. However, there were no significant differences in these parameters between both groups matched by FPG or severity of retinopathy. Multiple regression analysis to the basal GH level and GH responses during arginine infusion as criterion variables of various predictor variables (total 44 factors: biochemical laboratory data, indices of glucose and insulin response to oral glucose load, indices of glucose response to arginine, age, age of the onset, obese index, duration of retinopathy, neuropathy, and therapy) were performed in 86 patients using forward and backward method for variable selection. Basal plasma level of GH showed close positive association with therapy and proteinuria and negative association with age and obesity. Five of 6 indices of GH responsiveness showed significant relationship with retinopathy.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Growth hormone response to arginine administration in diabetics--with special reference to the multiple regression analysis in association with diabetic retinopathy]. 279 59

To gain insight into cellular events associated with the progression of obesity to diabetes, we have studied glucose metabolism and insulin responses in adipocytes from monkeys with spontaneous obesity. Over a 3- period, we studied animals which (A) remained relatively lean; (B) became obese (over 30 percent body fat) with normal glucose tolerance; (C) were obese and developed hyperinsulinemia (over 100 microU/ml); and (D) were obese and subsequently developed noninsulin-dependent diabetes (NIDDM) (fasting plasma glucose above 140 mg/dl and abnormal glucose tolerance test). Adipocyte glucose utilization, evaluated by conversion of 14-C-glucose to CO2 and lipids, was measured in the absence and presence of varying concentrations of insulin, using cells prepared from biopsy samples of subcutaneous abdominal fat. The major change in adipocyte metabolism was a decrease in basal and insulin-stimulated glucose utilization in NIDDM, relative to the enhanced responses observed in cells from the obese-hyperinsulinemic monkeys. Longitudinal studies of individual monkeys over 2-3 years led to the following additional observations regarding adipocyte glucose metabolism. Basal and insulin-stimulated glucose utilization dropped markedly as hyperinsulinemia progressed into diabetes. As impairments in glucose tolerance worsened in diabetes, adipocytes showed only a modest or negligible additional impairment in basal and insulin-stimulated glucose oxidation. Insulin binding was reduced in adipocytes from monkeys with obesity as compared to lean controls, and was similar in cells from monkeys with obesity and NIDDM. In the monkeys, obesity was initially associated with enhanced adipocyte metabolism. With the spontaneous development of NIDDM, glucose metabolism in adipocytes was depressed. The progression of metabolic events from hyperinsulinemia to NIDDM in monkeys includes cellular changes in insulin responses at the level of the adipocyte.
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PMID:Changes in insulin responses and binding in adipocytes from monkeys with obesity progressing to diabetes. 306 66

NIDDM appears to be a disease of complex aetiology. Although specific genetic markers for the disease have yet to be defined, there is clear evidence for genetic predisposition, with high concordance in monozygous twins. However, concordance is incomplete, and there are therefore additional, non-genetic, mechanisms which are responsible for increasing the risk of the disease in susceptible subjects. At the present time, the most plausible environmental precipitants appear to be the inter-related triad of obesity, low levels of habitual physical exercise and diet. The power of environmental determinants, and their interaction one with another, may also be subject to individual genetic determination, and may not act in a similar manner in all populations. Some non-Caucasian populations, which have undergone marked sociocultural change, are now extremely susceptible to NIDDM. This is probably the result of evolutionarily heightened genetic predisposition, compounded by strong environmental influence resulting from the recent changes in their human ecology. Since prevalence is strongly related to age, NIDDM also represents a growing problem to the world's industrialized societies, for many of which longevity is now the major demographic trend. Research into the aetiology of NIDDM must not only continue, it must also explore new directions, and attain greater scientific depth and sophistication, if it is to make a useful contribution to the eventual prevention and control of the disease.
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PMID:Aetiology. Non-insulin-dependent diabetes. 307 93

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