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)

The primary results of a three-year prospective, double-blind, placebo-controlled trial in non-insulin-dependent diabetic (NIDDM) patients show that an anti-hypertensive regimen, which includes the ACE inhibitor enalapril, preserves renal function to a greater extent than therapy with antihypertensive agents excluding ACE inhibitors (J Am Soc Nephrol 3:335, 1992). The influence of baseline urinary albumin excretion on the renal protective effects of enalapril treatment in these subjects was the objective of this further analysis. Adequate data were available in 121 patients of the 165 hypertensive NIDDM individuals studied [baseline glomerular filtration rate (GFR) 30 to 100 ml/min/1.73 m2]. Twenty-four hour urinary excretion of albumin (UAE), protein, urea nitrogen, creatinine and isotopically determined GFR were measured at baseline and six month intervals. Glycemic control and blood pressure regulation were assessed every three months. The rate of loss of GFR was significantly greater in patients with overt proteinuria at baseline (UAE > 300 mg/24 hr) as compared to patients with baseline sub-clinical proteinuria (UAE < or = 300 mg/24 hr). Antihypertensive treatment with enalapril preserved GFR significantly better (P < 0.01) in the patients with sub-clinical proteinuria at baseline (UAE < or = 300 mg/24 hr) than other antihypertensive treatments which excluded the ACE inhibitor. Furthermore, only 7% of the enalapril-treated group progressed to clinical albuminuria compared to 21% of control treated patients. Although the enalapril-treated group had a lower mean blood pressure during the maintenance period, no correlation between blood pressure (systolic, diastolic or mean arterial) and rate of change of GFR was observed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal protective effects of enalapril in hypertensive NIDDM: role of baseline albuminuria. 815 85

OBJECTIVE--To evaluate the frequency and correlates of glomerular hyperfiltration in NIDDM patients without overt proteinuria. RESEARCH DESIGN AND METHODS--A cross-sectional study was conducted. Seventy-one consecutive NIDDM patients attending an outpatient clinic, with Albustix-tested negative urine and a 24-h AER < 200 micrograms/min, were examined for long-term complications of diabetes. We measured their GFR (51Cr-EDTA single-injection method), 24-h AER (RIA), plasma creatinine, HbA1c, total cholesterol, triglycerides, urinary glucose, and urea. RESULTS--GFR above the upper limit of the normal range for age-matched control subjects (137.1 ml.min-1 x 1.73 m2) was present in 15 of 71 (21%) NIDDM patients. Subjects with normal and hyperfiltration did not differ in terms of age, sex distribution, BMI, duration of NIDDM, BP, AER, or frequency of long-term complications. Plasma glucose was significantly higher in subjects with hyperfiltration (mean [range]: 12.8 [4.3-18.7] vs. 8.7 [2.6-17.5] mM). HbA1c failed to reach statistical significance, although it tended to be higher in the group with hyperfiltration (10.4 [6.7-13.9] vs. 9.4 [4.2-16.5]%, P = 0.10). Age (rS -0.37, P = 0.002), FPG (rS 0.45, P < 0.0005), total cholesterol (rS -0.31, P = 0.008), and glycosuria (rS 0.40, P = 0.001) correlated significantly with GFR. In a stepwise multiple regression analysis, FPG, age, and total cholesterol emerged as significant correlates of the dependent variable GFR. CONCLUSIONS--Hyperfiltration occurred in 21% of NIDDM patients without overt proteinuria. FPG and age significant correlates of the GFR in these patients. Cholesterol is significantly (although only modestly) correlated with the GFR.
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PMID:Glomerular hyperfiltration in NIDDM patients without overt proteinuria. 842 64

Rapid growth large frame (RL, n = 61) or average growth medium frame (AM, n = 71) biotype heifers fed to achieve either moderate (MOD, .6 kg/d) or high ADG (HI, 1.0 kg/d) were used to determine whether puberty occurs at similar body composition or metabolic status. A heifer was considered pubertal after being detected in estrus and then forming a functional corpus luteum. Live animal estimates of body composition and blood samples for assessment of metabolic status were taken at 13 +/- .2 d after estrus for all heifers. Body composition and metabolic status were assessed every 56 d from 7 mo of age until puberty in a subset of 80 heifers representing all biotype-diet combinations. At puberty, 32 of these 80 heifers were slaughtered and physical and chemical composition of the empty body were determined. High-gain diet heifers were younger, heavier, taller, and more muscular (all P < .01) at puberty than MOD heifers. Slaughter measurements paralleled live animal estimates; bodies of HI and RL heifers contained more (P < .01) carcass and noncarcass components than those of MOD and AM heifers, respectively. Carcasses of RL and HI heifers were more (P < .05) muscular and fatter than AM and MOD heifers. At puberty, HI heifers had a greater (P < .01) mass of moisture, fat, and fat-free organic matter (FFOM) than MOD, whereas RL heifers had more moisture, ash, and FFOM than AM. Percentage of fat was greater (22.1 +/- 1.0 vs 1.0 vs 19.1 +/- 1.0; P < .05) and percentage of moisture was less (55.4 +/- .6 vs 58.1 +/- .6; P < .01) in bodies of HI than in those of MOD heifers. Concentrations of blood urea nitrogen and insulin were greater (P < .05) in HI than in MOD heifers. Diet did not influence concentration of IGF-I or glucose, and metabolic markers were unaffected by biotype. No dramatic changes in body composition or metabolic signals were detected before puberty. Puberty did not occur at similar body composition or metabolic status in all heifers.
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PMID:Body composition and metabolic profiles associated with puberty in beef heifers. 858 1

We investigated the effect of insulin on urinary excretion of phosphate in type II diabetes mellitus (DM) with respect to the absence or presence of renal insufficiency. A euglycemic-hyperinsulinemic clamp was performed in 37 type II DM patients. Subjects were divided into two groups: group A consisted of patients with serum creatinine levels less than 1.5 mg/dL (n = 22), and group B consisted of patients with serum creatinine levels of 1.5 mg/dL or greater (n = 15). Blood and urine samples were collected at the beginning and end of the clamp, and urinary excretion of phosphate was evaluated by calculating fractional excretion (FE-P). Tissue sensitivity to insulin in the whole body was expressed as the glucose infusion rate (M value) and that divided by steady-state plasma insulin levels (M/I ratio) during the last 30 minutes of the clamp. FE-P in group A patients significantly decreased during the clamp (from 9.46 +/- 0.67% before the clamp to 7.12 +/- 0.73% after the clamp, P < .004), whereas FE-P in group B patients did not change significantly during the clamp. The percent decrease of FE-P (decrease of FE-P during the clamp divided by FE-P before the clamp) in group A patients was significantly higher than in group B patients (22.5 +/- 7.0% and 2.5 +/- 5.1 %, respectively, P < .04). In all 37 patients, the percent decrease of FE-P was negatively correlated with blood urea nitrogen ([BUN] r = -.36, P < .05), serum creatinine (r = -.34, P < .05), and serum beta2-microglobulin (r = -.44, P < .01) and positively correlated with creatinine clearance (r = .570, P < .004), but it was not correlated with the M value or M/I ratio. These results showed that the kidneys of diabetic patients with renal insufficiency are insulin-insensitive in terms of phosphate transport, and the insulin insensitivity is related to the glomerular filtration rate but not to systemic insulin insensitivity. The percent decrease of FE-P on clamp study could be useful for assessing the insulin insensitivity of the kidney, which probably occurs primarily in the renal tubules.
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PMID:Effect of insulin on urinary phosphate excretion in type II diabetes mellitus with or without renal insufficiency. 863 55

The aim of this work was to ascertain if diabetes and obesity can affect gastric colonization by Helicobacter pylori. 59 hospitalized subjects with dyspepsia and endoscopic antral gastritis were selected. They were divided into three groups: I) 13 patients with normal body weight and without disease other than gastritis (control group); II) 15 patients with essential obesity of whom 10 had impaired glucose tolerance (IGT); III) 31 patients with type II diabetes mellitus, of whom 14 were obese. Three gastric biopsies were obtained from each patient for histologic examination and H. pylori detection by means of rapid urea test, culture and histological evidence of Helicobacter-Like Organisms (HLO). Age, sex, blood glucose, cholesterol, triglycerides, HDL-cholesterol, basal gastrine, duration of illness, body weight were statistically analysed. Differences between the three groups were not statistically significant. There was a higher prevalence of H. pylori infection both in obese and in diabetic patients with respect to control subjects. Prevalence became still higher in obese patients with impaired glucose tolerance. Among the three tests used for the detection of H. pylori, culture and rapid urea were reliable and specific, while the histologic test was highly sensitive but barely specific. Our data suggest that both obesity and type II diabetes may be associated with an increased incidence of H. pylori-colonization. This could be related to the reduced gastric motility observed in both pathologies and chemical changes in gastric mucosa following non-enzymatic glycosylation processes.
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PMID:Gastric infection by Helicobacter pylori and antral gastritis in hyperglycemic obese and in diabetic subjects. 872 11

We postulated whether interventions capable of restoring euglycemia would correct whole-body protein metabolism, shown previously to be elevated in hyperglycemic persons with non-insulin-dependent diabetes (NIDDM). The kinetics of protein metabolism were estimated in obese subjects with NIDDM in the hyper- and normoglycemic states during isoenergetic feeding and in the normoglycemic state induced by 4 wk of a very-low-energy diet (VLED) with constant protein intake. Seven NIDDM subjects [three males and four females with a body mass index (in kg/m2) of 39 +/- 2] were given a weight-maintaining, liquid formula providing 95 g protein/d for 15 d, followed in six subjects (two males and four females) for 27 d by a diet providing 1.7 MJ, 93 g protein derived from casein-soy, 13 g carbohydrate, 2 g fat, multivitamins and minerals, and a potassium bicarbonate supplement (32 mmol) per day. Exogenous insulin was given to achieve normoglycemia during the first 8 d of isoenergetic feeding. On days 6-8, 12-14, and 25-27, nitrogen flux rate was calculated from the urine [15N]urea enrichment by using the 60-h oral [15N]glycine method to obtain "integrated" feeding and fasting values. Rates of synthesis and breakdown were calculated from nitrogen flux. During isoenergetic feeding, normoglycemia was associated with more positive nitrogen balance (2.6 +/- 0.5 compared with -0.6 +/- 0.6 g N/d, P < 0.05); 18-23% lower nitrogen flux, and synthesis and breakdown rates (P < 0.05), and a 3% decrease in resting energy expenditure (P < 0.05). During the VLED, euglycemia was achieved but nitrogen balance, although it became less negative with time, never reached equilibrium. This was associated with significant (P < 0.05) decreases in the synthesis rate, resulting in net protein losses. Thus, the altered protein metabolism in moderately hyperglycemic NIDDM subjects was improved with exogenous insulin in doses sufficient to restore normoglycemia in the isoenergetic fed state, but it remained abnormal with a reduced non-protein energy intake. This suggests that protein metabolism is more sensitive to insulinization than was thought previously.
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PMID:Effect of glycemic control on the kinetics of whole-body protein metabolism in obese subjects with non-insulin-dependent diabetes mellitus during iso- and hypoenergetic feeding. 906 41

In Jamaica, malnutrition related diabetes mellitus (MRDM) presents the clinical picture of phasic insulin dependence. This study was undertaken to investigate nephropathic changes associated with this group of patients. Fourteen phasic insulin dependent diabetes mellitus (PIDDM) patients were compared with 10 insulin dependent (IDDM) and 10 non-insulin dependent (NIDDM) diabetes mellitus patients, and 10 normal controls. Each group was matched for age, sex, body mass index (BMI) and, in the case of the diabetic patient controls, duration of diabetes. Urinary microalbumin concentration was significantly (p < 0.05) higher in the PIDDM group (mean +/- SD: 153 +/- 48.3 mg/dl) than in the groups of NIDDM (35.7 +/- 9.6 mg/dl) or IDDM (38.6 +/- 15.8 mg/dl) patients. Serum urea and creatinine concentrations (mean +/- SE 7.6 +/- 1.0 mmol/l and 130.0 +/- 20.3 mumol/l, respectively) were higher in the PIDDM patients than in the NIDDM and IDDM groups. Confounding factors such as hypertension and urinary tract infections were excluded as causes for these differences. We conclude that PIDDM patients have more severe renal dysfunction than NIDDM patients and, since glycosylated haemoglobin concentrations are comparable in these groups, we attribute this to a renal insult due to malnutrition predating the onset of the PIDDM.
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PMID:Kidney function in phasic insulin dependent diabetes mellitus in Jamaica. 914 47

Oral antidiabetics (PAD) are still the most frequent pharmacotherapeutic intervention in NIDDM, characterized by insulin deficiency and in particular by insulin resistance in the liver and peripheral tissues. Depending on the site of action, they are divided into substances retarding carbohydrate breakdown in the small intestine (alpha-glucosidase inhibitors), substances stimulating B-cells of the islets of Langerhans (beta-cytotropic substances) and substances acting in the periphery. The authors discuss PAD, in particular SU and biguanides which have been used for treatment for some years and more recent preparations--acarbose (Glucobay) and miglitol. Attention is paid to perspective preparation which are in the research stage, among them in particular troglitazone which belongs into the group of substances which improve the sensitivity of insulin receptors (insulin sensitizers) which will soon be on the market. As to other possibilities the authors discuss the role of fatty acid oxidation and its inhibitors and new non-sulphonyl urea insulin secretagogues. All these preparations, despite certain limitations, offer exciting therapeutic perspectives. Further research will reveal to what extent this potential can be implemented in practice.
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PMID:[The present and future of treatment with oral antidiabetic agents]. 958 96

The authors examined 25 patients with diabetes mellitus type 2 (NIDDM) without vascular complications, treated by sulphonyl urea preparations, 12 hyperinsulinaemic (HI) non-diabetic subjects and 11 normoinsulinaemic healthy subject s. Patients with NIDDM and HI non-diabetics had significantly elevated PAI-1 levels which correlated with the C-peptide level (r = 0.519, p < 0.001), triacylglycerols (TG) (r = 0.685, p < 0.001), BMI (r = 0.607, p < 0.001) and levels of endothelial markers such as von Willebrand s factor and thrombomodulin (TM). In the group of patients with NIDDM no relationship of PAI-1 and C-peptide was found and a significant correlation was found with TM levels (r = 0.609, p = 0.001) and TG levels (r = 0.476, p = 0.046). The results suggest that the endothelial department has an effect on the regulation of PAI-1 levels in patients with NIDDM.
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PMID:[Plasminogen activator inhibitor (PAI-1) and markers of endothelial dysfunction in patients with diabetes mellitus]. 965 May 6

In the treatment of type 2 diabetes (NIDDM) we possess three groups of oral hypoglycaemic drugs: sulfonyl urea derivatives, biguanides (metformin) and alpha-glucosidase (acarbose) inhibitors. Oral treatment of diabetes has a favourable impact on the patients metabolic deviations but it involves also certain dangers and pitfalls. The side-effects of oral antidiabetics can be reduced to a minimum by respecting consequentially contraindications of administration of different preparations, knowledge of their mechanism of action and individual selection of a suitable antidiabetic for every patient.
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PMID:[Pitfalls in treatment with oral antidiabetic agents]. 975 Apr 81


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