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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Mexican Americans appear to have a strong genetic predisposition to insulin resistance, android obesity, and type II diabetes, apparently as a function of Native American genetic heritage. Theoretical considerations suggest that insulin resistance may be a primary factor that plays a causative role in the induction of both obesity and diabetes. Measures which promote optimal insulin sensitivity--chromium picolinate, brewer's yeast, soluble fiber supplements, metformin, very-low-fat diet, exercise training--may have value for preventing, treating, or retarding the onset of obesity and diabetes, and merit clinical evaluation in this regard. Correction of insulin resistance may also lessen cardiovascular risk, in part by reducing LDL cholesterol and improving risk factors associated with Syndrome X. These comments are likely to be valid for other Native American groups at high risk for diabetes.
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PMID:Insulin resistance in Mexican Americans--a precursor to obesity and diabetes? 828 93

Using the molecular scanning technique of single-stranded conformational polymorphism (SSCP), we have examined the exons encoding the insulin receptor gene in 26 patients with syndromes of insulin resistance. We found 27 variant sequences, 4 of which were mutations that altered an amino acid. One patient with the Rabson-Mendenhall syndrome was homozygous for a mutation in the extracellular alpha-subunit (Ser to Leu323), one type A insulin-resistant patient was heterozygous for Pro to Leu1178, and another type A insulin-resistant patient was heterozygous for a mutation in the COOH-terminus of the receptor (Arg to Gln1351). The previously reported, and probably functionally insignificant, variant Val to Met985 was detected in one patient. No missense or nonsense insulin receptor mutations were found in any patients whose insulin resistance was associated with gross obesity, lipoatrophy, or acromegaloid features. No missense or nonsense mutations were found in subjects with polycystic ovary syndrome or Syndrome X. Putting these findings in the context of other work in this field, we conclude that subjects with leprechaunism or Rabson-Mendenhall syndrome have a high probability of having a missense or nonsense insulin receptor mutation. Nonobese, nondysmorphic, severely insulin-resistant females with hirsutism, acanthosis nigricans, and menstrual disturbance (type A phenotype) have an intermediate probability of having this type of insulin receptor mutation. Although insulin receptor mutations have been occasionally described in other phenotypes of insulin resistance, the frequency of point mutations in the exons of the insulin receptor gene in patients with those phenotypes appears to be low.
Diabetes 1994 Mar
PMID:Molecular scanning of the insulin receptor gene in syndromes of insulin resistance. 831 8

The effects of Benfluorex administration on glucose tolerance have been examined in young and old Sprague Dawley rats. The ageing rats were used as a model of insulin resistance. Chronic oral administration of Benfluorex decreased triglycerides levels and normalized glucose tolerance in ageing rats, independently of effects on body weight. Acute intraportal administration of 0.45 mg/kg/h of Benfluorex for 30 min resulted in a 50% increase in glucose tolerance in old rats, but did not modify that in young rats. The improved glucose tolerance brought about by Benfluorex in an animal model of insulin resistance may suggest a wider therapeutic application in man, to include insulin resistant states as type II diabetes or Syndrome X.
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PMID:Improvement in glucose tolerance of insulin resistant rats after chronic or acute administration of benfluorex. 841 19

NIDDM has been postulated to be a component of a more generalized metabolic syndrome, Syndrome X, caused by insulin resistance. Although the components of the syndrome include glucose intolerance, hypertension, increased TG, and decreased HDL cholesterol, their relationship to insulin resistance and/or hyperinsulinemia is controversial. Recent investigations have shown racial differences in the relationship between insulin resistance and BP in nondiabetic populations. We assessed the relationship between insulin resistance and the other components of the syndrome in 37 black men and 53 black women with NIDDM. Insulin sensitivity was determined by measuring glucose disposal with the euglycemic insulin clamp technique with a 1 mU.kg-1.min-1 insulin infusion. We also determined fasting lipid profiles and BP. In this group of black men and women with NIDDM, 30% were insulin sensitive, and 70% were insulin resistant. No correlation existed between insulin sensitivity and sBP or dBP in either sex. Fasting serum TGs were inversely correlated with insulin sensitivity for both men (r = -0.401, P = 0.02) and women (r = -0.366, P = 0.008). Serum HDL cholesterol was highly correlated with insulin sensitivity for men (r = 0.421, P = 0.01) but not for women (r = 0.071, P = 0.62). Fasting serum TG levels and serum HDL-cholesterol levels were highly correlated in an inverse relationship in men (r = -0.368, P = 0.03), but not women (r = -0.199, P = 0.17). In summary, BP does not correlate with insulin resistance in blacks with NIDDM. Normal insulin sensitivity occurs in 33% of black men and 25% of black women with NIDDM.(ABSTRACT TRUNCATED AT 250 WORDS)
Diabetes 1993 Mar
PMID:Do blacks with NIDDM have an insulin-resistance syndrome? 843 15

Two follow-up studies were carried out to determine whether lower birthweight is related to the occurrence of syndrome X-Type 2 (non-insulin-dependent) diabetes mellitus, hypertension and hyperlipidaemia. The first study included 407 men born in Hertfordshire, England between 1920 and 1930 whose weights at birth and at 1 year of age had been recorded by health visitors. The second study included 266 men and women born in Preston, UK, between 1935 and 1943 whose size at birth had been measured in detail. The prevalence of syndrome X fell progressively in both men and women, from those who had the lowest to those who had the highest birthweights. Of 64-year-old men whose birthweights were 2.95 kg (6.5 pounds) or less, 22% had syndrome X. Their risk of developing syndrome X was more than 10 times greater than that of men whose birthweights were more than 4.31 kg (9.5 pounds). The association between syndrome X and low birthweight was independent of duration of gestation and of possible confounding variables including cigarette smoking, alcohol consumption and social class currently or at birth. In addition to low birthweight, subjects with syndrome X had small head circumference and low ponderal index at birth, and low weight and below-average dental eruption at 1 year of age. It is concluded that Type 2 diabetes and hypertension have a common origin in sub-optimal development in utero, and that syndrome X should perhaps be re-named "the small-baby syndrome".
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PMID:Type 2 (non-insulin-dependent) diabetes mellitus, hypertension and hyperlipidaemia (syndrome X): relation to reduced fetal growth. 843 55

We have previously demonstrated that women who had given birth to large infants had a six-fold increased risk of developing Type 2 (non-insulin-dependent) diabetes mellitus compared with a control group matched for age and parity. However, the patients were extremely obese which explained, in part, the increased risk. In the present investigation we studied whether the delivery of large infants correlated with risk factors for atherosclerotic vascular disease other than obesity and diabetes, and therefore could serve as early markers for syndrome X. The study consisted of 73 women who 20-27 years earlier had given birth to large infants weighing 4,500 g or more. Another group of 73 women matched for age, parity and BMI who had delivered infants weighing less than 4,500 g within a 3-month period served as a control group. Of these 73 patient/control pairs, 48 (66%) were able to participate in the investigation. Mean age was 52.2 years (range 40-66 years). No differences were noted for family history of diabetes and medication prescribed for vascular disease between the groups. An oral glucose tolerance test was performed and glucose, insulin and C-peptide at 0 and 2 h were estimated. Triglycerides, cholesterol, LDL and HDL cholesterol were analysed at baseline. We found no tendency towards hyperinsulinaemia and hyperglycaemia in the patients and both groups had the same relative increase in levels of insulin and C-peptide. No difference between the groups regarding manifest symptoms of vascular disease, either in blood pressure or in proteinuria were observed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Can the birth of a large infant predict risk for atherosclerotic vascular disease in the mother? 845 25

Studies of macrovascular disease in non-insulin-dependent diabetes (NIDDM) have shown a significant increase in peripheral vascular, coronary, and carotid artery disease in diabetics compared to non-diabetics. This prevalence appears to be related to insulin levels and to the degree of hyperinsulinemia as measured in the blood of these patients. Indeed, a cluster of markers, including hyperinsulinemia, insulin resistance, hypertension, dyslipoproteinemia, and a high waist-hip ratio, has been associated with NIDDM and increased risk for macrovascular disease. Variously described as Metabolic Syndrome or Syndrome X, this syndrome may be operative for many years before NIDDM is diagnosed. Given the complexity of Metabolic Syndrome, a single-factor intervention for preventing macrovascular disease in NIDDM is unlikely. However, it seems advisable to screen, on a regular basis, all patients presenting a pre-NIDDM state, as well as those with overt NIDDM, for pertinent cardiovascular risk parameters and for emerging macrovascular disease. It is suggested that any attempt to prevent macrovascular disease in subjects with glucose intolerance should aim at decreasing insulin resistance and hyperinsulinemia.
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PMID:Hyperinsulinemia and atherosclerosis. 854 11

The prevalence of hypertension in diabetes is significantly higher than in non-diabetics, perhaps twice as common. The excess is related to diabetic nephropathy, mainly in type 1 diabetes, to obesity, mainly in type 2 diabetes, but also to increased sympathetic activity. Furthermore, the increased prevalence of hypertension may relate to insulin resistance and its sequelae. Insulin resistance leads to hyperinsulinemia, relates to increased LDL and reduced HDL levels, causes the development of impaired glucose tolerance and type 2 diabetes and might also be causally related to the onset of hypertension. Syndrome X has relevant therapeutic implications in the management of hypertension. Hypertension is a major risk factor for large vessel disease in diabetics and also a risk factor for microangiopathy, particularly nephropathy. The incidence of atherosclerotic disease is dramatically increased in both type 1 and type 2 diabetics and is the major cause of morbidity and premature death mainly in patients with raised urinary albumin excretion. Thus, diabetics show a two-fold increased risk of coronary heart disease, 2-6 fold increased risk of stroke and a several-fold increased risk of peripheral vessel disease. Some evidence suggests that hypertension may be a risk factor for retinopathy, particularly its progression, but surely hypertension is a significant risk factor for nephropathy, accelerating its progression and perhaps even causing the onset of the glomerulopathy. The mechanisms by which hypertension might contribute to the evolution of both large vessel as well as small vessel disease is still unknown, although increased capillary leakage and vascular endothelium alterations might be important factors.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Hypertension and diabetes]. 856 58

The purpose of the study was to evaluate fasting endothelin-1 levels in subjects with syndrome X, in subjects with insulinoma, and in normal subjects. The single and synergistic contributions of insulin and triglyceride levels to endothelin-1 release were studied in normal subjects. This was achieved by the evaluation of endothelin-1 levels in response to an insulin bolus combined with a euglycemic clamp (protocol A) and during intralipid (test 1) or saline (test 2) infusions lasting 360 min (protocol B). In protocol B, a euglycemic two-step hyperinsulinemic (25 and 125 mU x kg-1 x h-1) clamp was started at 120 min. Subjects with syndrome X showed significantly higher endothelin-1 levels than normal subjects and subjects with insulinoma (7.22 +/- 0.89 vs. 2.61 +/- 0.38 and 2.49 +/- 0.24 pg/ml, P < 0.01). After an insulin bolus, endothelin-1 levels peaked at 10 min (3.71 +/- 0.96 pg/ml). The incremental area of endothelin-1 was significantly higher after insulin than after a saline bolus. In test 1, an acute increase in triglyceride levels significantly enhanced endothelin-1 levels, with were further increased by the synergistic contribution of high insulin and triglyceride levels. In test 2, endothelin-1 release was achieved at high insulin levels but remained significantly lower than in test 1. In conclusion, subjects with syndrome X showed higher endothelin-1 levels than normal subjects and subjects with insulinoma. These levels were reproduced in normal subjects by a simultaneous increase in insulin and triglyceride levels.
Diabetes 1996 Mar
PMID:Hypertriglyceridemia and hyperinsulinemia are potent inducers of endothelin-1 release in humans. 859 36

The paper reviews epidemiological studies published since 1989, not including ecological studies and addressing the relationship between the fetal environment and component elements of the chronic insulin resistance syndrome (syndrome X). Thirty papers have been recorded. Birth weight associated or not with other perinatal characteristics are studied in 24 articles. A relationship with further occurrence of hypertension (17 papers), dyslipemia (3), non insulin-dependent diabetes or altered glucose tolerance (8), or of a combination of these disorders (2), has been sought for. A negative relationship between birth weight and these disorders is found in adults, inconstantly in children. Some findings support a mechanism implying nutritional condition during pregnancy. Methodology inaccuracies jeopardize the validity of the conclusions drawn. The interpretation of a causal relationship between fetal environment and insulin resistance is compared to alternative assumptions relating to genetic mechanisms or selection biases.
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PMID:[Fetal environment and coronary ischemia risk: review of the literature with particular reference to syndrome X]. 876 85


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