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

Glucose intolerance is often associated with pancreatitis. Pancreatitis-induced diabetes represents a different clinical syndrome than type I and type II diabetes mellitus. Patients with pancreatitis-induced diabetes may be extremely sensitive to exogenous insulin, rarely develop ketoacidosis, and rarely exhibit classic diabetic complications, such as retinopathy, nephropathy, or accelerated vasculopathy. Pancreatic polypeptide (PP) deficiency has been implicated in the defect of glucose homeostasis found after pancreatitis. This study evaluated intravenous and oral glucose tolerance and insulin response to glucose loading, in the setting of pancreatitis, with and without short-term PP replacement. Dogs (n = 7) underwent pancreatic duct ligation (PDL) and were studied with and without PP infusion (2 micrograms/kg/hr) before PDL and at 1 week, 6 weeks, and 4 months after PDL by means of intravenous and oral glucose tolerance tests. Basal and bombesin-stimulated PP levels at 4 months after PDL were subnormal, verifying PP deficiency in these animals with pancreatitis. PP levels during PP infusion reproduced normal postcibal levels, averaging 897 +/- 40 pg/ml. Glucose tolerance, expressed as the glucose decay constant for the intravenous glucose tolerance tests and as the integrated glucose response for the oral glucose tolerance tests, deteriorated over time and was not improved by acute PP replacement. The integrated insulin response to glucose was not affected by PP. The acute infusion of PP at a dose that reproduces normal postprandial PP levels fails to improve glucose tolerance or augment insulin release in this model of pancreatitis-induced diabetes.
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PMID:The effect of pancreatic polypeptide infusion on glucose tolerance and insulin response in longitudinally studied pancreatitis-induced diabetes. 219 57

Several epidemiological studies have reported that the regional distribution of body fat is a significant and independent risk factor for cardiovascular disease (CVD) and related mortality. Although these associations are well established, the causal mechanisms are not fully understood. Numerous studies have, however, shown that specific topographic features of adipose tissue are associated with metabolic complications that are considered as risk factors for CVD such as insulin resistance, hyperinsulinemia, glucose intolerance and type II diabetes mellitus, hypertension, and changes in the concentration of plasma lipids and lipoproteins. The present article summarizes the evidence on the metabolic correlates of body fat distribution. Potential mechanisms for the association between body fat distribution, metabolic complications, and CVD are reviewed, with an emphasis on plasma lipoprotein levels and plasma lipid transport. From the evidence available, it seems likely that subjects with visceral obesity represent the subgroup of obese individuals with the highest risk for CVD. Although body fat distribution is now considered as a more significant risk factor for CVD and related death rate than obesity per se, further research is clearly needed to identify the determinants of body fat distribution and the causal mechanisms involved in the metabolic alterations. It appears certain, however, that an altered plasma lipid transport is a significant component of the relation between body fat distribution and CVD.
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PMID:Regional distribution of body fat, plasma lipoproteins, and cardiovascular disease. 219 40

This report presents an overview of the prevalence, characteristics, morbidity, mortality, and risk factors for noninsulin-dependent diabetes (NIDDM) in Blacks and Whites in the United States. Data are drawn primarily from national surveys, but the report also includes the few clinical studies that have differentiated the two races. NIDDM constitutes 90-95% of all diabetes in the United States and is more prevalent in Black Americans than in Whites. Diabetes prevalence increases with age for both races and reaches 26% among Blacks aged 65-74 years compared with 18% among Whites. Rates of diabetes among persons aged 20-74 years are 30% higher in White women, 70% higher in Black men, and 100% higher in Black women, compared with White men. Approximately half of diabetes is undiagnosed in both races. White and Black diabetics are similar with regard to age, duration of diabetes, and diabetes therapies, although Blacks of both sexes are more obese than their White counterparts. Rates of vision loss, amputations, and renal disease are 1.5-4 times higher in Blacks than in Whites, although prevalence of hypertension is about equal in the two races. Blacks and Whites see the same physician specialists for their diabetes, but Whites have approximately 40% more visits to office-based physicians each year. Diabetes-specific mortality has declined significantly in the past decade and may now be lower in Black than in White diabetics. Risk factors for diabetes, including age, sex, obesity, and family history of diabetes, all operate within both race groups and probably interact with each other. The effect of gender and family history on rates of diabetes is similar in Blacks and Whites. Blacks have higher rates of diabetes at each obesity level, indicating that obesity alone cannot explain the differential in prevalence between the races. Impaired glucose tolerance (IGT), a strong risk factor for development of diabetes, increases with age in all race/sex groups except for Black women older than 54 years in whom rates of IGT, decline, possibly because of conversion of IGT to diabetes.
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PMID:Noninsulin-dependent diabetes mellitus in black and white Americans. 219 51

Non-insulin-dependent diabetes mellitus (NIDDM) is being increasingly diagnosed as its importance as a risk factor for the development of cardiovascular disease continues to be recognised. Good metabolic control remains a major goal of drug therapy as it decreases the severity and incidence of diabetic complications. Many drugs have been known to interfere with glucose control, either in a beneficial or, more commonly, in a deleterious fashion. Unfortunately in many instances drug-induced effects have not been looked at specifically in NIDDM. Thiazide diuretics have been shown to cause a deterioration in glucose control not only in the general population but especially in patients who have impaired glucose tolerance. While the effect appears less with potassium supplementation and the lower dosage employed nowadays, thiazide diuretics are best avoided in diabetic patients. Loop diuretics have been reported to reduce glucose control to a lesser extent than thiazides. Although indapamide would appear not to interfere with blood sugar control in NIDDM, higher doses that cause potassium loss may cause a deterioration. beta-Adrenoceptor antagonists have been reported to cause a rise in blood sugar and glycosylated haemoglobin in NIDDM. The effect may be more marked in patients on oral hypoglycaemic agents as opposed to diet alone and in those on concomitant thiazide diuretics. The greatest effect was seen with propranolol, and the least with cardioselective and the less lipophilic beta-blockers. It is of interest that alpha-blockade with prazosin seems to antagonise beta-adrenoceptor blocker-induced deterioration in glucose control. The calcium antagonists have differing effects which may be structure related. In some, but not all, studies use of the dihydropyridines such as nifedipine has been associated with a deterioration in glucose control in NIDDM. Long term studies are needed to assess definitively their effect on glucose control. Verapamil, on the other hand, has in 1 small study been found to have a beneficial effect on glucose control in NIDDM. Centrally acting alpha-agonists such as the antihypertensive drug clonidine have not been shown to result in a deterioration in glucose control when used in NIDDM, although there are isolated case reports. Long term therapy with the more specific agonist guanfacine was reported in 1 uncontrolled study to have a beneficial effect on glucose tolerance in NIDDM. Uncontrolled studies suggest that phenothiazines may aggravate diabetic control. The significance of a number of recent observations is not fully clear.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Effects of drugs on glucose tolerance in non-insulin-dependent diabetics (Part I). 220 83

Although the primary defect(s) responsible for the development of type 2 diabetes still is unknown, several recent cross-sectional and longitudinal studies have clarified the sequence of events leading to type 2 diabetes. Relatives of type 2 diabetic patients, who have normal glucose tolerance, are characterized by hyperinsulinemia and insulin resistance compared to relatives with no family history of diabetes. In individuals with impaired glucose tolerance, insulin resistance is more severe than in those with normal glucose tolerance. The acute insulin response is lower in subjects with impaired glucose tolerance than in those with normal glucose tolerance but the decrease in the acute insulin response is similarly related to increases in plasma glucose as in normal subjects. A high postprandial insulin concentration, as well as the degree of insulin resistance, predicts the transition of glucose tolerance from impaired to diabetic. These data suggest that hyperinsulinemia and insulin resistance rather than insulin deficiency predict the subsequent development of type 2 diabetes in individuals genetically susceptible to the disease. As insulin resistance can be ameliorated with therapeutic measures such as weight loss and exercise, apparently healthy individuals with high insulin concentrations and a family history of type 2 diabetes might be regarded as a high-risk group which will require intensive attention from health care professionals.
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PMID:Evidence for a primary role of insulin resistance in the pathogenesis of type 2 diabetes. 220 84

Non-insulin-dependent diabetes mellitus (NIDDM) is characterized by insulin resistance and beta-cell dysfunction. This review focuses on the beta-cell, what defects occur when and why. Two major anatomic observations have been made in NIDDM. The beta-cell mass is mildly reduced, especially when obesity is taken into account. Also, amyloid deposits are frequently observed in the islets. It is unclear whether these changes are genetically mediated or result secondary to the loss of glucose homeostasis. Many studies have looked at some aspect of insulin secretion in NIDDM, and two types of distinct abnormalities have been described. Early on, there is a marked disruption in pulsatile insulin delivery, which is potentially an important contributor to the insulin resistance. It is unclear whether the loss of pulsatile delivery is acquired or genetically induced. Later, after glucose intolerance has started, several other secretory abnormalities develop coincident with loss of beta-cell glucorecognition. The net result is further deterioration in timing of insulin delivery and postprandial hyperglycemia. A second important consequence of the glucose blindness is that the inherent compensatory beta-cell mechanisms that guard against hyperglycemia are bypassed. We propose that the loss of glucose responsiveness is a direct result of an elevated glucose concentration (so-called glucotoxicity) and have generated substantial data in rat models that support this idea. The logical conclusion is that beta-cell function in NIDDM can be maximized by achieving the best metabolic control possible.
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PMID:Natural history of beta-cell dysfunction in NIDDM. 222 13

The mean additional energy requirement for pregnancy has been calculated at 285 kcal daily and it reflects the energy needs for production of the fetoplacental unit and for the maternal physiological adaptations to pregnancy. In practice there is considerable variation in energy requirement due to alterations in maternal energy expenditure. Optimal energy intakes are dictated also by the pre-pregnancy maternal weight. The outcome of pregnancy is improved in the underweight mother by an intake which produces a weight gain in pregnancy of approximately 14 kg, whereas a rise of only 7 kg may be optimal for the obese mother. Obesity with or without diabetes is associated with macrosomia and other problems and it is sensible to attempt to limit weight gain in pregnancy at a time when maternal motivation is high. Diabetes in pregnancy may arise in patients with pre-existing NIDDM or IDDM, but more commonly it is diagnosed for the first time during pregnancy and it usually disappears after delivery (gestational diabetes). Recent evidence suggests that gestational diabetes has a strong genetic component and is usually NIDDM precipitated early in life by the pregnancy. Both gestational diabetes and NIDDM are characterized by insulin deficiency and by insulin resistance. Long-term follow-up studies have demonstrated that NIDDM or impaired glucose tolerance develop in later life in 50-70% of women with previous gestational diabetes. The adverse effects of pregnancy on the mother with pre-existing diabetes may be minimized by good diabetic control as may be adverse effects on the fetus and neonate of diabetes in the mother. An increased incidence of fetal malformations persists in pregnancies with pre-existing maternal diabetes. Diabetes of any form may be associated with neonatal hypoglycaemia. The aim of therapy is to produce maternal normoglycaemia throughout pregnancy by dietary measures and insulin treatment if required. Women with pre-existing diabetes should tighten their blood glucose control from before conception. Optimization of insulin therapy and diet are required for IDDM and most NIDDM women will require insulin treatment in pregnancy. Gestational diabetics require diet and possibly insulin. Most pregnancies now proceed to term.
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PMID:Diabetes and diet in pregnancy. 224 97

An altered mineral metabolism has been described both in insulin dependent and non-insulin dependent diabetes mellitus. In order to investigate if a disturbed mineral homeostasis was an early feature in the development of diabetes, 52 middle-aged men who all had recently developed an impaired glucose tolerance (IGT) were compared to healthy control persons. The IGT subjects showed higher levels of serum calcium (2.38 +/- 0.081 mmol/l (SD) vs 2.35 +/- 0.065 in controls) but similar levels of plasma ionized calcium indicating an increased protein binding of serum calcium in IGT. Serum magnesium was significantly lower in the IGT subjects (0.79 +/- 0.060 mmol/l vs 0.85 +/- 0.065, p less than 0.001) while serum phosphate was unaltered. This study demonstrates indices of an impaired mineral metabolism in IGT subjects similar in characteristics to what has previously been reported in manifest diabetes mellitus suggesting that an alteration of mineral homeostasis could be part of a primary event.
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PMID:Indices of mineral metabolism in subjects with an impaired glucose tolerance. 227 19

Forty-nine patients with tropical calcific pancreatitis (TCP), 51 insulin-dependent diabetics (IDDMs), 87 non-insulin-dependent diabetics (NID-DMs), and 66 nondiabetic controls were studied to evaluate their exocrine pancreatic function by measurement of serum immunoreactive trypsin (IRT, normal for white caucasians from the U.K. of 140-414 micrograms/L), pancreatic isoamylase (PIA, normal of 35-125 U/L), and fecal chymotrypsin (FCT, normal of greater than 6.6 u/g). The majority of patients were studied within 1 year of diagnosis. TCP subjects included 7 nondiabetics, 6 with impaired glucose tolerance (IGT-TCP), and 36 diabetics [fibrocalculous pancreatic diabetes (FCPD)]. There was evidence of active pancreatitis (IRT greater than 800 micrograms/L) and partial preservation of function in nondiabetic TCP subjects [median IRT of 220 micrograms/L (range of 102-1,360 micrograms/L), FCT of 2.2 u/g (range 0.7-12.8 u/g)] and also in IGT-TCP subjects [IRT of 370 micrograms/L (range of 30-1,360 micrograms/L), FCT of 4.2 u/g (range of 1-38 u/g)]. FCPDs showed severely diminished exocrine function [IRT of 50 micrograms/L (range of 0-184 micrograms/L), FCT of 0.23 u/g (range of 0-10.4 u/g)]; none showed IRT greater than 800 micrograms/L. IDDMs and NIDDMs also showed diminished exocrine pancreatic function in approximately 30 and approximately 10%, respectively. Controls showed a wide range of IRT and FCT concentrations; IRT concentrations tended to be higher than those reported in white Caucasians from the U.K. Three controls, one IDDM, and two NIDDMs showed "pancreatic" IRT concentrations in the absence of symptoms. PIA concentrations were diminished in FCPD but were similar in IDDM and NIDDM subjects compared to controls.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Exocrine pancreatic function (serum immunoreactive trypsin, fecal chymotrypsin, and pancreatic isoamylase) in Indian diabetics. 228 Oct 79

The term Impaired Glucose Tolerance (IGT) has replaced the term Subclinical Diabetes (SD). It corresponds to a grey zone between normal glucose tolerance (GT) and diabetic glucose intolerance which by definition can be determined only by an oral glucose tolerance test. Pathogenetically, and impaired glucose tolerance constitutes a risk factor for the formation of atherosclerosis and in about 30% of cases represents a pre-stage of diabetes mellitus. No mortality statistics are as yet available for insureds with impaired glucose tolerance. We may, however, assume with good reason that their relative mortality lies between the comparable values of insureds with normal glucose tolerance and those with type 2 diabetes. The relative mortality of type 2 diabetes is calculated on the basis of the American Medical Impairment Study 1983 and the Swiss Re study on diabetes mellitus and the relative mortality of insureds with impaired glucose tolerance is then determined on that basis. Finally, a possible course of action for the risk assessment of applicants with impaired glucose tolerance is proposed and the expected extra mortality rates are given.
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PMID:[Life expectancy and risk assessment in decreased glucose tolerance (subclinical diabetes)]. 229 Dec 66


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