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Query: UMLS:C0011849 (diabetes)
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Urinary albumin, measured by radioimmunoassay, was evaluated as a method to assess early renal impairment in 76 insulin (IDD) and 36 noninsulin (NIDD)-dependent diabetic patients. Mean albumin excretion in IDD and NIDD patients was significantly higher at 23 and 12 micrograms/100 ml glomerular filtrate (GF) respectively, compared to 4 micrograms/100 ml GF in normal subjects (P less than 0.001 and P less than 0.05). Abnormal albumin excretion from 20 to 200 micrograms/100 ml GF was observed in 30% of IDD patients (P less than 0.001) and 15% of NIDD patients (P less than 0.03). Albumin excretion was significantly increased in hypertensive IDD and NIDD patients. Significant correlations between albumin excretion and age, duration of diabetes and creatinine clearance were observed, but albumin excretion did not correlate with hemoglobin A1C. These data indicate that (1) 30% of IDD patients not clinically recognized as having renal impairment have abnormal albumin excretion, (2) albumin excretion may reflect renal impairment, since albumin excretion levels independently correlate with duration of diabetes and hypertension in both diabetic subgroups and to glomerular function in NIDD patients, and (3) measurement of urinary albumin by radioimmunoassay may be the most sensitive test to evaluate early renal disease in diabetes.
Diabetes Res Clin Pract 1986 Apr
PMID:The interrelationships of radioimmunoassayable urinary albumin, renal function and diabetes. 372 Apr 98

49 diabetics (D) (26 IDD and 23 NIDD) were compared to 32 controls (C). Absence of ischemic cardiopathy (IC) was confirmed by routine investigations and noninvasive cardiovascular techniques, including an exercise ECG using 12 leads and a thallium 201 scintigraphy. Our results show: a) a prolonged mean isovolumetric relaxation time (IVRT) as studied by the M mode echocardiography and phonomechanography: D = 0,10 sec +/- 0,04; C = 0,05 sec +/- 0,02; p less than 0,0001; b) a reduced mean EF slope: D = 97,48 +/- 37,08 mm / sec; C = 125,68 +/- 34,35; p less than 0,005; c) a high mean Weissler index (ratio of PEP to LVET): D = 40 +/- 0,08; C = 33 +/- 0,05; p less than 0,01. IVRT and EF slope abnormalities are related to increased myocardial stiffness and impaired LV compliance. In the absence of changes in preload and afterload, the high Weissler index reflects impaired contractility of the myocardium. These abnormalities are related neither to the duration of diabetes nor to the presence or severity of the complications. With the M mode echocardiography, mean diastolic and systolic thickness of the septum is greater in D with retinopathy than in C (p less than 0,005 and p less than 0,03 respectively); mean diastolic and systolic thickness of the posterior wall is greater in NIDD than in C (p less than 0,001 and p less than 0,025). We conclude that there is evidence of left ventricular functional abnormalities specific to diabetes and unrelated to IC and hypertension. Our findings support the hypothesis that they may be due to metabolic disorders and/or myocardial microangiopathy.
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PMID:[Existence of asymptomatic changes in left ventricular function in the diabetic. Noninvasive study]. 400 44

There are residual ambiguities between the two main current glycaemic definitions of the categories of DM, IGT and normal GT which should be resolved. IGT is clearly a highly heterogeneous category and could with advantage be resolved into its identifiable subsets though adequate data for this is not yet available. The concept of insulin dependency requires clearer definition for operational purposes. Biochemical parameters (e.g. C-peptide responses) may help. Attempts to combine clinical manifestations and pathogenic mechanisms in a single classification (e.g. IDDM/NIDD versus Type I/Type II) should be handled with care. If the term Type I is to be retained, it should be applied to a defined pathogenic process, not to a clinical type of DM. The term Type II is inadequately defined at present. IDDM and NIDDM, clinical descriptive terms, may be provoked by a variety of pathogenic mechanisms (i.e. they are 'heterogeneous'). They could be subclassified by mechanism (when known). More visibility should be given in classification to non-Europid forms of DM (e.g. 'Tropical or 'Nutritional' DM). A staging dimension should be recognised in classifications of DM. Future classifications will benefit from the incorporation of the presence or absence of susceptibility/resistance factors to diabetes itself or to its severe long term sequelae. There remain uncertainties about the definitions and clinical implications of gestational DM (and gestational IGT) not discussed above. It should be accepted that different user groups may need different subclassification of diabetes and glucose intolerance to meet their specific requirements and so long as this is made clear and definitions are adequate this should not be a problem. However, for the present, all groups should accept the proposed glycaemic definitions of DM or IGT for the purposes of comparability.
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PMID:Limitations and problems of diabetes classification from an epidemiological point of view. 403 18

The pancreatic islet can be viewed as an integrator of nutrient, neural, and hormonal signals. In normal people, glucose directly stimulates insulin release and also plays a key role as a potentiator of nonglucose stimulants of the B-cells. In patients with non-insulin-dependent diabetes mellitus (NIDDM), the direct effect of glucose on insulin secretion is markedly impaired. However, as hyperglycemia develops, basal insulin levels and insulin responses to nonglucose signals are maintained in many NIDD patients by the potentiating effect of hyperglycemia. Both acute and chronic administration of sulfonylurea drugs results in enhanced B-cell sensitivity to the potentiating effect of glucose. During sulfonylurea therapy this effect initially causes an increase in insulin level. However, as the glucose level falls during therapy the insulin level may tend to return toward pretreatment values, thereby masking the improvement of B-cell function. In NIDD patients with mild to moderate hyperglycemia (fasting plasma glucose less than 200 mg/dl), chronic sulfonylurea therapy results in the maintenance of near-normal insulin levels, but at a lower plasma glucose level. In patients with more severely impaired B-cell function, whose insulin levels before therapy are subnormal despite marked hyperglycemia, there is a net absolute increase in insulin levels during chronic sulfonylurea administration. Thus, some NIDD patients may show an increase in basal insulin levels during chronic sulfonylurea therapy while others may not; however, all patients who respond to sulfonylureas demonstrate increased B-cell sensitivity to glucose. Acute and chronic sulfonylurea treatment also results in a suppression of glucagon levels, an effect that may be secondary to the enhancement of B-cell function. The fall of plasma glucose during chronic sulfonylurea therapy is associated with a decrease in hepatic glucose production in NIDD patients. The magnitude of this effect is correlated with the degree of enhancement of basal insulin secretion. Thus, chronic sulfonylurea therapy clearly enhances pancreatic islet function in patients with NIDDM. We postulate that the major antihyperglycemic action of sulfonylurea therapy is mediated by this pancreatic effect.
Diabetes Care
PMID:Acute and chronic effects of sulfonylurea drugs on pancreatic islet function in man. 637 26

Non-insulin-dependent diabetes ( NIDD ) was obtained in adult rats following a neonatal streptozotocin injection. Rats with NIDD exhibited a chronic low-insulin response to glucose in vivo, slightly elevated basal plasma glucose values (less than 2 g/l) and low pancreatic insulin stores (50% of the controls). Glucagon secretion was studied in this model, in vivo and in vitro using the isolated perfused pancreas technique. Normal basal plasma glucagon levels were observed in the fed state and were in accordance with normal basal glucagon release in vitro. The pancreatic glucagon stores were normal in the diabetics. In experiments with the perfused pancreas, the increased glucose concentration suppressed glucagon release as readily in the diabetics as in the controls. Moreover 5.5 mM glucose suppressed glucagon release stimulated by 19 mM arginine to the same extent in both groups. These data indicate that the suppression of A cell function by glucose is normal in rats with NIDD . Theophylline and isoproterenol also produced normal glucagon release in diabetics. By contrast, the glucagon secretion in response to arginine was lower in the diabetics. This was observed either in vivo (arginine infusion) or in vitro in the presence or the absence of glucose in the perfusate. But in the presence of theophylline the response to arginine was normalized in the diabetics. Impairment of A cell function of the diabetics is not limited to recognition of amino-acids, since acetylcholine evoked a lower glucagon response in the diabetics than in the controls. These defects are different from those described in their B cells.
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PMID:Glucagon secretion in rats with non-insulin-dependent diabetes: an in vivo and in vitro study. 672 97

The mechanisms contributing to the impairment in glucose metabolism in non-insulin-dependent diabetes mellitus, insulin-dependent diabetes mellitus, and diabetic ketoacidosis are summarized in Table 2. Impaired insulin secretion is characteristic of patients with IDD and DKA. In contrast, insulin secretion in NIDD may be normal, increased, or decreased. Peripheral tissue resistance to the action of insulin is present in all three diabetic conditions; it is moderate in NIDD and IDD and severe in DKA. Basal hepatic glucose production in NIDD and IDD can be either normal or increased, and correlates closely with the fasting plasma glucose concentration. In DKA, HGP is elevated. Suppression of HGP by insulin is normal in NIDD and IDD but severely impaired in DKA. Hepatic glucose uptake following oral glucose is decreased in NIDD; hepatic uptake of ingested glucose has not been examined in IDD and DKA.
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PMID:Insulin resistance: a universal finding in diabetic states. 682 Sep 36

A comparative study was carried out on B cell response to alternative intravenous glucagon (1.0 mg) and intravenous glucose (0.33 g per kg body weight) in healthy non-obese persons (c-NOb), healthy obese persons (C-Ob), non-obese non-insulin-dependent diabetics (NIDD-NOb) and obese non-insulin-dependent diabetics (NIDD-Ob). Each group comprised ten subjects. C-peptide (CP immunoassay using antiserum M 1230) and IRI in the serum were measured for each test. After glucose load in B-cell responses were significantly lower in both the diabetic groups than in the normal groups. After glucagon injection there were no significant differences in IRI and CP levels between NIDD-NOb and C-NOb, however, significantly lower levels of serum CP were noted among NIDD-Ob in comparison to C-Ob with a lack of these differences in IRI levels. This phenomenon is well reflected by the molar IRI/CP ratio expressed as a percentage. In the fasting state IRI accounted in C-Ob for 8.8 +/- 3.5 per cent of CP, while in NIDD-Ob for up to 25. +/- 10.4 percent of CP (P = 0.0004). In the latter group of patients, the IRI/CP ratio after glucagon reached the highest values (over 30 per cent) observed in this study. These data suggest the important role in insulin disposal played by the liver in non-insulin-dependent diabetes associated with obesity. Another explanation for these data is that more proinsulin is secreted in this group of patients as compared to other groups.
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PMID:Serum C peptide and IRI levels after administration of glucagon and glucose in non-insulin-dependent diabetics. 704 Jan 96

In a retrospective investigation 228 obese persons with healthy metabolism and diabetics (NIDD) were invited to a check-up 4-10 years after a reduction of weight which was performed during a clinical treatment in the 2nd Medical Clinic of Halle University. 95 patients did not comply with the invitation, 9 patients had died in the meantime. Among the 24 obese persons examined were 9 patients with NIDD. In other 19 patients a diabetic metabolic disturbance had become manifest in the meantime. 78 obese persons underwent a clinical examination, among them 9 NIDD. 60 patients had a normal and 18 a pathological carbohydrate tolerance. Of these 18 patients in 9 patients an up to now unknown diabetes mellitus could be proved. The obesity coincides with a relatively high rate of disturbed carbohydrate tolerance and a larger proportion of manifest diabetics compared with the normal population. In the own group of patients the morbidity of diabetes among the obese persons increases from 10.5 to 30% after on an average 7 years. Obese persons who had essentially exceeded their initial weight in the meantime and show further metabolic disturbances are particularly endangered.
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PMID:[Studies on the incidence of diabetes mellitus in obese patients]. 713 89

In Seattle, Washington, the prevalence of diabetes was 20% in second-generation (Nisei) Japanese-American men and 16% in Nisei women 45-74 years old, while the prevalence of impaired glucose tolerance (IGT) was 36% in Nisei men and 40% in Nisei women. Hyperglycemia was less and duration of diabetes shorter in women. Related to diabetes and IGT in Nisei were higher fasting plasma insulin levels and central (visceral) adiposity. Prevalence of diabetes was low among the younger (34-53 years old) third-generation (Sansei) men and women. Among self-reported non-diabetic Sansei, however, prevalence of IGT was 19% in men and 29% in women, and IGT was associated with both increased fasting plasma insulin levels and more visceral fat, suggesting that many Sansei are at risk of future diabetes. An important lifestyle factor in the development of NIDD in Japanese Americans appeared to be dietary saturated (animal) fat. Another factor may be physical inactivity. In Japanese-American women, menopause also appeared to be an important risk factor. These risk factors may be related to fostering the accumulation of visceral fat and the development of insulin resistance. Five-year follow-up examinations performed in non-diabetic Nisei men and women have yielded additional information concerning the prognosis of IGT. Of those women who were IGT at baseline, 34% were diabetic at follow-up while 17% returned to normal. In men who had been IGT at baseline, 18% were diabetic at follow-up while 36% returned to normal. Over the 5-yr follow-up interval, proportionally more women progressed from normal to IGT (54%) then went from IGT to normal (17%). For men, roughly equal proportions went from normal to IGT (37%) as from IGT to normal (36%). It would therefore appear that greater proportions of Nisei women are progressing to IGT and to NIDD than are Nisei men. This observation may be related to the increased risk of developing central obesity and insulin resistance following menopause. Prevalence of cardiovascular disease (hypertension, peripheral vascular disease, and/or coronary heart disease) was increased in Japanese Americans with IGT and NIDD. Neuropathy and retinopathy were associated only with NIDD.
Diabetes Res Clin Pract 1994 Oct
PMID:Diabetes and diabetes risk factors in second- and third-generation Japanese Americans in Seattle, Washington. 785 32

Extrapancreatic activity of the sulfonylurea, glipizide, was evaluated in the neonatal streptozotocin-induced rat model of noninsulin-dependent diabetes. Two day old Wistar rats were given a bolus of streptozotocin (90 mg/kg i.p.) to cause noninsulin-dependent diabetes; these animals became severely glucose intolerant and eventually developed a cardiomyopathy characterized by reduced heart rate, contractility and cardiac output. Male littermates injected with citrate buffer served as nondiabetic controls. At four weeks of age, the nondiabetic and NIDD rats were administered by gavage either glipizide (2.5 mg/kg) or the methyl cellulose vehicle. Throughout the treatment protocol, no difference in the degree of glucose intolerance was observed between the glipizide-treated and vehicle-treated animals. Glipizide therapy also was ineffective in improving plasma insulin levels, which were significantly depressed in the diabetic group. Yet, animals treated with glipizide for one year exhibited improved myocardial contractile function relative to the vehicle-fed or ad lib fed diabetic animals. Heart rate was significantly elevated and there was a tendency for both the rate of relaxation and contractility to be elevated in sulfonylurea-treated group. Glipizide also reduced the degree of insulin resistance in the heart. Since these changes occur in the absence of changes in glucose tolerance or insulin levels, the heart appears to be very sensitive to the direct effects of the sulfonylureas.
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PMID:Effects of chronic glipizide treatment on the NIDD heart. 840 18


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