Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of this study was to evaluate the influence of endogenous insulin levels and of insulin administration on coronary heart disease (CHD) and on mortality in a cohort of patients with long-standing non-insulin-dependent diabetes mellitus (type 2). In a cross-sectional study, 93 patients (known duration 17 +/- 8 years, mean+/-SD) with poor metabolic control (glycosylated hemoglobin, HbA1C 9.3%+/-2.09%) were evaluated for CHD, for insulin release (C-peptide), for clinical and metabolic parameters including body mass index (BMI), smoking habits, arterial blood pressure (BP), blood lipids, kidney function, and proteinuria. Life status was ascertained 5 years later by direct examination or through death certificates. At entry, 54 out of 93 patients had CHD; after 5 years, 25 patients had died. Comparisons performed on patients of the same age range showed that patients with CHD (34 vs 24) had a greater BMI, higher diastolic BP, higher creatinine, triglyceride and uric acid levels, and higher fasting and i.v. glucagon-stimulated C-peptide release. By logistic stepwise regression analysis, fasting C-peptide and triglycerides were independently associated with CHD. In the follow-up study, surviving patients (39 vs 19) showed at baseline lower triglyceride and creatinine levels, were less frequently affected by CHD, and received lower doses of insulin; by logistic stepwise regression analysis, presence of CHD, dose of insulin, and creatinine levels were independent risk factors for mortality. These data indicate that in patients with long-standing type 2 diabetes mellitus and poor metabolic control, CHD and overall mortality are related to insulin release and to insulin administration, suggesting that markers of insulin resistance represent additional risk factors for CHD and for mortality. Reduction of insulin resistance, together with achievement of good metabolic control, might prevent morbidity and mortality in long-standing type 2 diabetes mellitus.
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PMID:Markers of insulin resistance are associated with cardiovascular morbidity and predict overall mortality in long-standing non-insulin-dependent diabetes mellitus. 962 90

A previous study had shown an increased prevalence (83%) of diverticula among patients with autosomal dominant polycystic kidney disease (ADPKD) with end-stage renal disease (ESRD) compared with other ESRD patients without ADPKD (32%). Others have also suggested an increased risk for diverticular complications in renal transplant recipients with ADPKD. To determine whether there was an increased occurrence of diverticula among non-ESRD patients with ADPKD, we studied 55 patients with ADPKD who were not receiving renal replacement therapy compared with 12 unaffected family members (non-ADPKD) and 59 random patients who had undergone barium enemas (control [C]). No study patient had a history of diverticular disease. All patients underwent a double-contrast barium enema after administration of glucagon. The occurrence, number, location, and size of diverticula were noted. There was no significant difference among the three groups in regard to sex (men: ADPKD, 42% versus non-ADPKD, 42% versus C, 37%) or age (ADPKD, 49.3 +/- 0.7 versus non-ADPKD, 51.2 +/- 2.1 versus C, 49 +/- 1 years). There was no significant difference in the percentage of patients with diverticula (ADPKD, 47% versus non-ADPKD, 58% versus C, 59%), the percentage with only right-colon diverticula (ADPKD, 5% versus non-ADPKD, 17% versus C, 5%), the mean number of diverticula in patients with diverticulosis (ADPKD, 13.8 versus non-ADPKD, 7.9 versus C, 9.9 diverticula), or the size of the largest diverticula (ADPKD, 9.5 versus non-ADPKD, 10.4 versus C, 10.5 mm). There was no significant difference in these variables between the patients with ADPKD with a creatinine clearance greater than 70 mL/min/1.73 m(2) (n = 25) or less than 70 mL/min/1.73 m(2). This study does not show the greater prevalence of diverticular disease in non-ESRD patients with ADPKD compared with the general population. Thus, patients with ADPKD need not be considered at greater risk for diverticular disease than the general population.
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PMID:Evaluation of colonic diverticular disease in autosomal dominant polycystic kidney disease without end-stage renal disease. 1056 Nov 42

Hyperzincuria is a common feature in diabetic patients, which is still not understood. Based on the above consideration, the aim of the present study was to investigate the renal handling of zinc in insulin-dependent diabetes mellitus (IDDM) patients. The glomerular filtration rate, urinary zinc excretion, zinc clearance, zinc clearance/creatinine clearance ratio, zinc tubular reabsorption, glycosuria, plasma glucose, C-peptide, glucagon, and cortisol were investigated in 10 normal individuals (Group C1 and Group C2, respectively) and 10 IDDM patients (Group E1: hyperglycemic and glycosuric and Group E2: normoglycemic and aglycosuric) during placebo or venous zinc tolerance test. The results showed that urinary zinc excretion and renal zinc clearance were increased after zinc injection in normal individuals (Group C2) and IDDM patients (Groups E1 and E2) when compared with normal individuals-placebo (Group C1). However, these renal parameters were statistically more significant in the hyperglycemic and glycosuric diabetics (Group E1). Because patients in Group E1 had the lowest plasma C-peptide levels and showed a strong negative correlation between CZn++/Ccr ratio and this hormone, we suggest that in this setting insulin inhibits urinary zinc excretion.
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PMID:Renal handling of zinc in insulin-dependent diabetes mellitus patients. 1136 78

The urinary excretion of insulinotropic glucagon-like peptide 1 (GLP-1) was investigated as an indicator of renal tubular integrity in 10 healthy subjects and in 3 groups of type 2 diabetic patients with different degrees of urinary albumin excretion rate. No significant difference emerged between the groups with respect to age of the patients, known duration of diabetes, metabolic control, BMI, or residual beta-cell pancreatic function. Endogenous creatinine clearance was significantly reduced under conditions of overt diabetic nephropathy, compared with normo and microalbuminuric patients (p < 0.01). Urinary excretion of GLP-1 was significantly higher in normoalbuminuric patients compared to controls (490.4 +/- 211.5 vs. 275.5 +/- 132.1 pg/min; p < 0.05), with further increase under incipient diabetic nephropathy conditions (648.6 +/- 305 pg/min; p < 0.01). No significant difference resulted, in contrast, between macroproteinuric patients and non-diabetic subjects. Taking all patients examined into account, a significant positive relationship emerged between urinary GLP-1 and creatinine clearance (p = 0.004). In conclusion, an early tubular impairment in type 2 diabetes would occur before the onset of glomerular permeability alterations. The tubular dysfunction seems to evolve with the development of persistent microalbuminuria. Finally, the advanced tubular involvement, in terms of urinary GLP1 excretion, under overt diabetic nephropathy conditions would be masked by severe concomitant glomerular damage with the coexistence of both alterations resulting in a peptide excretion similar to control subjects.
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PMID:Urinary excretion of glucagon-like peptide 1 (GLP-1) 7-36 amide in human type 2 (non-insulin-dependent) diabetes mellitus. 1156 Dec 19

Effects of different feeding frequencies on growth performance, preprandial metabolic parameters, and endocrine traits were studied in calves up to 28 d after birth and respective postprandial changes were investigated on d 3 and 7. Calves were fed with a computer-programmed automate that allowed frequent daily intakes (GrA; n = 7) or were fed twice daily by bucket (GrB; n = 7) the same daily amounts (pair-feeding) of colostrum and milk. Weight gains did not differ significantly between groups. Plasma protein was higher (P < 0.01) from d 14 to 28 in GrB than in GrA. Plasma glucose increased postprandially in GrB on d 3 and 7 but in GrA only on d 3, and there was a significant treatment x time interaction on d 3 and 7 after feed intake. For plasma triglycerides there was a significant postprandial treatment x time interaction on d 3, and triglycerides were higher (P < 0.05) in GrA than in GrB before feed intake on d 7. For insulin concentrations on d 7 the treatment x time interaction was significant and concentrations 8 h after feed intake were higher (P < 0.05) in GrA than GrB. For concentrations of growth hormone on d 7 during an 8-h period the treatment x time interaction was significant and concentrations from 320 to 340 min after feed intake were higher (P < 0.05) in GrB than in GrA. Plasma IGF-I concentrations were higher (P < 0.05) in GrA than in GrB on d 7. The hematocrit and concentrations of immunoglobulin G, albumin, urea, creatinine, L-lactate, nonesterified fatty acids, cholesterol, glucagon, and thyroxine did not differ between groups. In conclusion, feed intake at high frequency by an automate transiently changed some metabolic and endocrine traits (glucose, triglyceride, insulin, and IGF-I) but had no significant effects on growth performance during the first 4 wk of life.
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PMID:Growth performance and metabolic and endocrine traits in calves pair-fed by bucket or by automate starting in the neonatal period. 1207 36

To determine the effect of octreotide acetate on urinary excretion of uric acid and plasma concentration of uridine, we subcutaneously administered octreotide acetate (1 microg/kg of body weight) to 5 healthy subjects. Ninety minutes after administration, octreotide acetate increased the plasma concentration of uridine by 15% and decreased the plasma concentration of glucagon by 24% and that of insulin to below the detection limits. In addition, octreotide acetate decreased the urinary excretion of uric acid, sodium, and chloride by 60%, 40%, and 38%, respectively, at 1 hour after administration. However, octreotide acetate did not affect the concentrations of hypoxanthine, xanthine, uric acid, cyclic AMP in plasma, lactic acid and pyruvic acid in blood, urinary excretion of hypoxanthine and xanthine, or creatinine clearance. From these results, we speculated that octreotide acetate decreases the urinary excretion of uric acid by decreasing the concentration of glucagon and/or urinary excretion of sodium, and increases the plasma concentration of uridine via decreased concentrations of glucagon and insulin.
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PMID:Effect of octreotide acetate on the plasma concentration and urinary excretion of uridine and purine bases. 1208 Dec 31

Streptozotocin (STZ) is often used to induce diabetes in animal models. However, morbidity associated with STZ and its ability to induce diabetes vary with different dosages among different animal species, including nonhuman primates. To find an optimal dose of STZ that would cause diabetes with minimal toxicity, we compared low and high doses of STZ. Male cynomolgus monkeys (3-6 years old) were given a single dose of 100 mg/kg (high dose, 4 animals) or 55 mg/kg (low dose, 20 animals) of STZ. Blood glucose levels, intravenous glucose tolerance test (IVGTT), pancreatic biopsies, liver function tests (LFTs), liver biopsies, kidney function tests, and kidney biopsies were performed periodically. Animals from both groups developed diabetes within 24 h after administration of STZ. Serum C-peptide levels in both groups decreased from 2 to 8 ng/mL before STZ to between 0.01 and 0.6 ng/mL after STZ. Animals with the high dose of STZ developed transient vomiting within minutes after injection. During the first week after STZ injection, high-dose animals developed elevated LFTs, BUN and creatinine. In contrast, low-dose animals had normal liver and kidney function tests. Histological analysis showed that animals given the high dose of STZ developed marked steatosis of the liver and tubular injury in the kidneys, whereas animals given the low dose of STZ had normal-looking liver and kidney histology. The pancreatic islets in both groups were indistinguishable by immunoperoxidase staining for insulin, and showed either no insulin-positive cells or rare insulin-positive cells. Glucagon staining was normal. Over time, low-dose diabetic monkeys remained persistently hyperglycemic with negligible C-peptide stimulation by intravenous glucose. We conclude that low-dose STZ at 55 mg/mL successfully induces diabetes in cynomolgus monkeys with minimal liver and kidney toxicity.
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PMID:The effect of low versus high dose of streptozotocin in cynomolgus monkeys (Macaca fascilularis). 1261 80

The composition of the raw legume Phaseolus vulgaris L. var. athropurpurea (PhVa) and its effects on the metabolism of young growing rats have been evaluated. The levels of protein, unsaturated fatty acids, carbohydrate, fibre and bioactive factors present in PhVa were comparable with those in other Phaseolus vulgaris varieties. However, the lectins of PhVa were predominantly of the leucoagglutinating type, and concentrated in the albumin protein fraction. Rats fed a diet (110 g total protein, 16.0 MJ/kg) in which PhVa meal provided about half of the protein excreted high levels of N in faeces and urine, and grew more slowly, than rats fed a high-quality control diet (ad libitum or pair-fed). Small intestine, large intestine and pancreas weights were increased (by almost 100 %, P<0.05), whilst skeletal muscle, thymus and spleen weights were reduced. Blood insulin (16.20 v. 0.50 mU/l, P<0.05, thyroxine, glucose, protein (60.5 v. 48.3 g/l, P<0.05) and LDL-cholesterol were lowered, whilst glucagon (155.3 v. 185.4 ng/l, P<0.05), triiodothyronine and urea were elevated, as were urinary urea, creatinine and glucose. These changes in the local (gut) and systemic metabolism of rats were probably mediated primarily by lectins in PhVa, which were concentrated in the albumin protein fraction, whereas in many other Phaseolus vulgaris lines they are distributed across the globulin and albumin fractions.
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PMID:Local (gut) and systemic metabolism of rats is altered by consumption of raw bean (Phaseolus vulgaris L var athropurpurea). 1262 26

The hepatorenal syndrome (HRS) is related to vasoconstriction of the renal cortex induced by systemic hypovolemia that follows splanchnic vasodilatation as the primary event in the cascade of hemodynamic changes associated with portal hypertension. We evaluated the effects of octreotide, a splanchnic vasoconstrictor, on HRS in cirrhotic patients. We compared the effects of octreotide infusion (50 microg/h) to placebo using a randomized, double-blind, cross-over design over 2, 4-day periods. Nineteen patients were included, and 14 patients could complete the 2 phases of the study (group 1: placebo first; n = 8 and group 2: octreotide first; n = 6) The end point of the study was to evaluate improvement in renal function as defined by a 20% decrease in serum creatinine value after a 4-day treatment as compared with baseline. In all the patients, a normal central venous pressure was maintained by daily intravenous administration of 2 units of albumin. The 2 groups were similar with regard to demographic data and liver and kidney function parameters at baseline. Improvement in renal function was observed in 2 patients after the placebo and 1 patient after octreotide infusion in group 1 and in 2 patients after octreotide infusion and 1 patient after placebo in group 2 (P = not significant). In addition, treatment with octreotide infusion did not result in significant changes in creatinine clearance, daily urinary sodium, plasma renin activity, plasma aldosterone and glucagon levels, or renal and mesenteric artery resistance indices as measured by Doppler ultrasonography. In conclusion, the present study demonstrates that, under our experimental conditions, octreotide infusion combined with albumin is not effective for the treatment of HRS in cirrhotic patients.
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PMID:Octreotide in hepatorenal syndrome: a randomized, double-blind, placebo-controlled, crossover study. 1283 7

Glucagon-like peptide 1 (GLP-1) and gastric inhibitory polypeptide (GIP) are important factors in the pathogenesis of type 2 diabetes and have a promising therapeutic potential. Alterations of their secretion, in vivo degradation, and elimination in patients with chronic renal insufficiency (CRI) have not yet been characterized. Ten patients with CRI (aged 47 +/- 15 years, BMI 24.5 +/- 2.2 kg/m(2), and serum creatinine 2.18 +/- 0.86 mg/dl) and 10 matched healthy control subjects (aged 44 +/- 12 years, BMI 24.9 +/- 3.4 kg/m(2), and serum creatinine 0.89 +/- 0.10 mg/dl) were included. On separate occasions, an oral glucose tolerance test (75 g), an intravenous infusion of GLP-1 (0.5 pmol. kg(-1). min(-1) over 30 min), and an intravenous infusion of GIP (1.0 pmol. kg(-1). min(-1) over 30 min) were performed. Venous blood samples were drawn for the determination of glucose (glucose oxidase), insulin, C-peptide, GLP-1 (total and intact), and GIP (total and intact; specific immunoassays). Plasma levels of GIP (3-42) and GLP-1 (9-36 amide) were calculated. Statistics were performed using repeated-measures and one-way ANOVA. After the oral glucose load, plasma concentrations of intact GLP-1 and intact GIP reached similar levels in both groups (P = 0.31 and P = 0.87, respectively). The concentrations of GIP (3-42) and GLP-1 (9-36 amide) were significantly higher in the patients than in the control subjects (P = 0.0021 and P = 0.027, respectively). During and after the exogenous infusion, GLP-1 (9-36 amide) and GIP (3-42) reached higher plasma concentrations in the CRI patients than in the control subjects (P < 0.001 and P = 0.0033, respectively), whereas the plasma levels of intact GLP-1 and GIP were not different between the groups (P = 0.29 and P = 0.27, respectively). Plasma half-lives were 3.4 +/- 0.6 and 2.3 +/- 0.4 min for intact GLP-1 (P = 0.13) and 5.3 +/- 0.8 and 3.3 +/- 0.4 min for the GLP-1 metabolite (P = 0.029) for CRI patients vs. healthy control subjects, respectively. Plasma half-lives of intact GIP were 6.9 +/- 1.4 and 5.0 +/- 1.2 min (P = 0.31) and 38.1 +/- 6.0 and 22.4 +/- 3.0 min for the GIP metabolite (P = 0.032) for CRI patients vs. healthy control subjects, respectively. Insulin concentrations tended to be lower in the patients during all experiments, whereas C-peptide levels tended to be elevated. These data underline the importance of the kidneys for the final elimination of GIP and GLP-1. The initial dipeptidyl peptidase IV-mediated degradation of both hormones is almost unaffected by impairments in renal function. Delayed elimination of GLP-1 and GIP in renal insufficiency may influence the pharmacokinetics and pharmacodynamics of dipeptidyl peptidase IV-resistant incretin derivatives to be used for the treatment of patients with type 2 diabetes.
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PMID:Secretion, degradation, and elimination of glucagon-like peptide 1 and gastric inhibitory polypeptide in patients with chronic renal insufficiency and healthy control subjects. 1498 49


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