Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011860 (type 2 diabetes)
 57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

There are striking similarities between Cushing's syndrome and the 'metabolic syndrome X' since both are characterised by hypertension, insulin resistance, glucose intolerance, hyperlipidaemia, and central obesity. The possibility that cortisol contributes to the associations between multiple risk factors for cardiovascular disease was rejected when it was demonstrated that there was no elevation in cortisol secretion or circulating concentration in patients with essential hypertension or type 2 diabetes mellitus. However, in recent years the enormous variability in tissue sensitivity to cortisol has become apparent. We have measured tissue sensitivity to glucocorticoids using an assay of skin vasoconstriction and have demonstrated its relationship with high blood pressure, insulin resistance, glucose intolerance, and hypertriglyceridaemia. Our data suggest that the increase in dermal glucocorticoid sensitivity is not a secondary phenomenon and may be explained by increased glucocorticoid receptor affinity together with impaired inactivation of cortisol by 11 beta-hydroxysteroid dehydrogenase. Importantly, we have not found that enhanced peripheral glucocorticoid sensitivity is associated with compensatory suppression of cortisol secretion, so that the maintenance of normal circulating cortisol concentrations in patients with cardiovascular risk factors may be paradoxical and inappropriate.
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PMID:Abnormal glucocorticoid activity in subjects with risk factors for cardiovascular disease. 896 30

Hyperuricemia is often associated with obesity, hypertension and dyslipidemia, and is thought to be a risk factor for cardiovascular disease, thereby making resemblance to the insulin resistance syndrome. Our data showed a low, but significant correlation between serum uric acid concentration and the degree of insulin resistance (GIR) estimated by euglycemic hyperinsulinemic clamp method in 67 subjects with combined normal glucose tolerance and IGT(r = -0.278, p < 0.05). Plasma HDL-C and TG levels were also correlated with uric acid levels. One hundred sixty NIDDM patients who had undergone the clamp study were stratified into 5 groups according to the serum uric acid level. In the top quintile (UA : 7.8 +/- 0.8 mg/dl), BMI, male prevalence, plasma TG, HDL-C, fasting IRI, and total IRI response(0 + 60 + 120 min) during meal tolerance test were significantly higher, while age and GIR value tended to be lower without significance compared with those in the bottom quintile (UA : 3.4 +/- 0.5 mg/dl). These results, which are in agreement with the previous studies, support the notion that elevated serum uric acid is a feature of insulin resistance syndrome.
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PMID:[Hyperuricemia and insulin resistance]. 897 8

Diabetes mellitus needs to be managed early to prevent the onset and progression of complications. Diet and exercise may not be sufficient to achieve and maintain good glycemic control. Currently, no pharmacologic agent addresses all of the fundamental abnormalities in the pathogenesis of type II diabetes mellitus. However, the newer agents do not exacerbate the hyperinsulinemia that often occurs with type II diabetes, and they may help reduce the risk of cardiovascular disease that is associated with high insulin levels. Two of these agents, metformin and acarbose, have recently become available in the United States for the treatment of type II diabetes. With the availability of agents that differ in their mechanisms of action and side effect profiles, regimens can be individualized to address the variety of pathophysiologic abnormalities in type II diabetes. For this purpose, agents can be used alone or in combination.
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PMID:Recent advances in the treatment of type II diabetes mellitus. 933 56

Microalbuminuria has been reported to precede the development of NIDDM and to be a risk marker for cardiovascular disease. Therefore, the present study investigated the relationship between urinary albumin excretion rate (UAER) and the degree of insulin resistance in Japanese subjects with impaired glucose tolerance (IGT). Thirty-three normotensive IGT subjects were divided into three groups and twenty hypertensive IGT subjects were divided into two groups according to the degree of insulin resistance (GIR value) estimated by the euglycemic hyperinsulinemic clamp method. UAER was significantly higher in the lower GIR group in normotensive subjects (highest GIR group, 6.6 +/- 0.9 mg/24 h; intermediate group, 10.5 +/- 3.0 mg/24 h; lowest group, 21.3 +/- 3.8 mg/24 h; P<0.01 between highest and both of the other groups), but not in hypertensive subjects. The lowest GIR was associated with higher fasting plasma insulin, increased insulin response to glucose, higher plasma triglyceride and uric acid, and lower high-density-lipoprotein cholesterol, but not with increased creatinine clearance rate in normotensive subjects. A similar tendency was also found in hypertensive subjects. It is concluded that UAER is related to insulin resistance in normotensive subjects with IGT through a mechanism other than glomerular hyperfiltration.
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PMID:Urinary albumin excretion rate is related to insulin resistance in normotensive subjects with impaired glucose tolerance. 906 67

The aim of this study was to compare, by gated radionuclide angiography, systolic and diastolic ventricular function in insulin-dependent (IDDM) and non-insulin-dependent (NIDDM) diabetic patients without overt cardiovascular disease. The study population consisted of 20 IDDM patients (15 male, 5 female; 40.7 +/- 10.3 years), 14 NIDDM patients (9 male, 5 female; 47.0 +/- 7.5 years) and 12 healthy subjects (7 male, 5 female; 41.5 +/- 6.3 years) as a control (C) group. The duration of diabetes (DD) and glycosylated hemoglobin (HbA1C) levels were significantly higher in the IDDM patients. The ventricular ejection fraction and peak ejection rate (PER) were assessed by gated radionuclide left ventriculography and were similar in three groups, while the peak filling rate (PFR) was lower in the NIDDM patients compared to the IDDM patients (p < 0.05) and controlled healthy subjects (p < 0.01, IDDM = 3.39 +/- 1.14; NIDDM = 2.65 +/- 0.83; C = 3.55 +/- 0.73), the time to PFR was significantly more prolonged in the NIDDM group than in the IDDM (p < 0.05) and C groups (p < 0.05, NIDDM = 162 +/- 26; IDDM = 140 +/- 28; C = 142 +/- 23). The PFR/PER ratio was near the normal value (approximately equal to 1) in the IDDM patients and controlled subjects, while in the NIDDM patients it was reduced (approximately equal to 0.84 +/- 0.18). Seven IDDM and 4 NIDDM patients had borderline signs of cardiovascular autonomic neuropathy, unrelated to DD, HbA1C and scintigraphic parameters. Left ventricular systolic performance was substantially normal and similar in both the IDDM and NIDDM patients. Ventricular diastolic filling was impaired in the NIDDM patients, as shown by the decrease in PFR and in particular in the PFR/PER ratio. Our radionuclide data suggest that the NIDDM patients had a prevalent abnormality of ventricular diastolic performance, with respect to the IDDM patients, although the latter patients had higher DD and HbA1C values.
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PMID:Left ventricular function in insulin-dependent and in non-insulin-dependent diabetic patients: radionuclide assessment. 909 15

Non-insulin-dependent diabetes mellitus (NIDDM) constitutes about 85% of all cases of diabetes in developed countries and it has now reached epidemic proportions in many developing nations, as well as disadvantaged groups in developed countries, e.g., Mexican- and African-Americans and Australian Aborigines and Torres Strait Islanders. The diagnosis of NIDDM is usually made after the age of 50 years in Europids, but it is seen at much younger age in these high prevalence populations, which also include Pacific Islanders, Native Americans, and migrant Asian Indians and Chinese. There is enormous variation in NIDDM prevalence between populations, and exceptionally high rates have been documented in populations who have changed from a traditional to a modern lifestyle, e.g., American Pima Indians, Micronesians, and other Pacific Islanders, Australian Aborigines, migrant Asian Indians, and Mexican-Americans. Over the next decade, following the initial phase of the NIDDM epidemic, macro- and microvascular complications will emerge as a major threat to future public health throughout the world with huge economic and social costs. The major cause of death in NIDDM is macrovascular disease (coronary artery, peripheral vascular, and cerebrovascular), which accounts for at least two-thirds of NIDDM mortality. A key strategy in reducing macrovascular disease lies in the better understanding of the Deadly Quartet or Metabolic Syndrome. New data suggest that hyperleptinemia rather than hyperinsulinemia may play an important and central role in the genesis of the cardiovascular disease risk factor cluster that constitutes the Metabolic Syndrome.
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PMID:The global epidemiology of non-insulin-dependent diabetes mellitus and the metabolic syndrome. 910 89

Non-insulin-dependent diabetes mellitus (NIDDM) is associated with approximately two fold increase in coronary heart disease (CHD) in men and fourfold increase in CHD in women. In most studies, the duration of diabetes and severity of glycemia are only weakly related to CHD in NIDDM, suggesting that the prediabetic period may be important for the increased CHD in NIDDM subjects. Both hyperinsulinemia and/or insulin resistance predict the development of NIDDM. A number of studies have shown that increased cardiovascular risk factors (especially high triglyceride, blood pressure, and small dense low-density lipoprotein (LDL) and low high-density liproprotein (HDL) cholesterol) precede the onset of NIDDM. Recent data from the San Antonio Heart Study suggest that the atherogenic pattern of cardiovascular risk factors is more marked in prediabetic women than in prediabetic men, thus partially explaining the higher risk of CHD in prediabetic women than in prediabetic men. The atherogenic changes in cardiovascular risk factors appear to be mainly due to increased hyperinsulinemia and insulin resistance in nondiabetic subjects. Interventions to reduce cardiovascular disease in NIDDM subjects should emphasize the primary prevention of NIDDM and very aggressive treatment of traditional cardiovascular risk factors in prediabetic subjects. Treatment of hypertension and dyslipidemia in high-risk patients for NIDDM should avoid agents that further worsen insulin resistance (nicotinic acid, beta blockers, and thiazides), as subjects with hypertension and dyslipidemia are already at increased risk of NIDDM.
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PMID:The prediabetic problem: development of non-insulin-dependent diabetes mellitus and related abnormalities. 910 90

Lipid peroxidation may be important in the development of cardiovascular disease, a common cause of mortality and morbidity in non-insulin dependent diabetes mellitus (NIDDM). We assessed the degree of lipid peroxidation by measuring plasma malondialdehyde, as thiobarbituric acid reacting substances (TBARS), in 23 non-insulin diabetic patients. Plasma levels of standardised alpha-tocopherol (vitamin E), lipid content of whole plasma and lipoprotein fractions, glycosylated haemoglobin, glycosylated low density lipoprotein (LDL) and fasting blood glucose were also measured. On completion of the baseline studies patients randomly received either fish oil or matching olive oil capsules in a double blind crossover fashion for 6 weeks followed by a 6 week washout period and a final 6 week treatment phase. Studies, identical to the initial baseline studies, were performed at the end of the of the active treatment periods at 6 and 18 weeks. Treatment with olive oil did not change levels of TBARS, vitamin E or indices of glycaemic control compared with baseline. Total cholesterol and triglyceride (TG) content of plasma and lipoprotein fractions were not significantly altered. Treatment with fish oil resulted in elevation of TBARS (P < 0.001) and reduction of vitamin E (P < 0.01) compared with baseline and olive oil treatment. Plasma cholesterol was unchanged. A reduction in plasma TG compared with baseline occurred but failed to reach significance (P =0.07). Changes in apo B containing lipoproteins induced by fish oil failed to reach significance. No significant changes were observed in concentration or composition of high density lipoprotein (HDL). Fish oil treatment showed no change in glycaemic control as assessed by glycosylated haemoglobin and LDL although a rise in fasting blood glucose just failed to reach significance (P = 0.06). Lipid peroxidation in NIDDM can be exacerbated by dietary fish oil. This potentially adverse reaction may limit the therapeutic use of fish oils in such patients.
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PMID:Effect of dietary fish oil supplementation on peroxidation of serum lipids in patients with non-insulin dependent diabetes mellitus. 912 1

Non-insulin-dependent diabetes mellitus (NIDDM) is increasing in incidence as the population in most countries ages. Multiple pathology is common in the elderly, and cardiovascular disease is usually present at diagnosis. Patients who develop NIDDM at age 65 years may live long enough to develop microvascular complications. Others who are frail and have multiple pathologies may require treatment to prevent both symptomatic hyperglycaemia and dehydration, whilst avoiding hypoglycaemia. The goals in the management of NIDDM in elderly people are the prevention of complications and the relief of symptoms. Treatment must be tailored to the individual's expectations and should be reviewed regularly with the changing circumstances of aging. If dietary measures fail to control glucose levels, antihyperglycaemic sulphonylureas are the most frequently prescribed form of treatment. However, concern over the potential of these drugs to cause hypoglycaemia limits the choice to second generation sulphonylureas, agents that preserve the first phase of insulin release and have non-biologically active metabolites that are promptly eliminated. The biguanide agent metformin is also appropriate in elderly obese patients with NIDDM who do not have renal, liver or cardiac failure. The combination of a sulphonylurea and metformin can be effective in patients in whom insulin would otherwise be required. Novel compounds such as acarbose and the thiazolinediones may also be useful in the treatment of older diabetic patients.
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PMID:Oral antihyperglycaemics. Considerations in older patients with non-insulin-dependent diabetes mellitus. 914 53

We tried to elucidate the possible relationship between lipoprotein (a) levels and coronary heart disease by assessing the presence of lipoprotein (a) covariates in NIDDM. We selected 41 type 2 diabetic patients with coronary heart disease and 82 type 2 diabetic patients free from cardiovascular disease. They were adjusted for age, sex and duration of diabetes. Routine chemical analysis was carried out using standard procedures, HbA1c by HPLC and lipoprotein (a) and urinary albumin excretion rate by immunonephelometry. No difference has been found in lipoprotein (a) levels between both groups of patients (18 [144.25] mg/dl in cases vs. 23 [197.25] mg/dl in controls (median [range]), Mann Whitney U-test, P > 0.1). No association has been found between coronary heart disease and lipoprotein (a) levels greater than 30 mg/dl (Pearson's chi 2, P > 0.1). Significant and independent linear relationships have been found between the square root of lipoprotein (a) levels, serum creatinine and total cholesterol (multiple r2: 0.15, P < 0.001). Patients treated with insulin had greater square root of lipoprotein (a) levels, even after adjusting for serum creatinine and total cholesterol (5.87 +/- 0.35 vs. 4.76 +/- 0.36 (mean +/- S.E.), ANCOVA, P < 0.05). These data do not show an association between symptomatic coronary heart disease and lipoprotein (a) in NIDDM. Significant and independent relationships have been found between this variable and serum creatinine, total cholesterol and insulin therapy.
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PMID:Lack of association of lipoprotein (a) with coronary heart disease in Spaniard type 2 diabetic patients. 917 69


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