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

One hundred and twenty-nine (97 M, 32 F) previously untreated non-insulin-dependent diabetic patients were studied. Meal and glucose (75 g) tolerance tests were performed on two separate days with glucose, C-peptide and insulin levels estimated during each with the inclusion of growth hormone during the meal test. In addition glycosylated haemoglobin (HbA1) and plasma creatinine levels were determined. Clinical evaluation included detailed ophthalmological examination following mydriasis. Differences between retinopaths (n = 21) and non-retinopaths (n = 108) were FPG 13.7 vs 11.6 (mmol/l) (p less than 0.01); HbA1: 12.9 vs 11.3 (%) (p less than 0.01); BMI: 25.2 vs 29.4 (kg/m2) (p less than 0.001); age 56.8 vs 52.4 (yr) (ns); creatinine: 91.2 vs 88.4 (mumol/l) (ns); systolic blood pressure: 152.4 vs 143.9 mmHg (ns); diastolic blood pressure 87.9 vs 87.7 mmHg (ns); fasting growth hormone: 4.6 +/- 0.9 vs 2.4 +/- 0.3 (mU/1) (p less than 0.01). Multivariate logistic analysis however revealed that systolic blood pressure in conjunction with the insulin response gave the most significant correlation with retinopathy. No significant correlation was observed with age, sex, diastolic blood pressure, creatinine, family history or smoking. The effect of disease duration could not be evaluated. B-cell function appears central to microvascular complications in non-insulin dependent diabetes mellitus.
 ...
PMID:Retinopathy in newly presenting non-insulin-dependent (type 2) diabetic patients. 307 31

Several studies report increased growth hormone (GH) responses to provocative stimuli in patients with diabetic retinopathy. We studied GH responses to 1 microgram/kg body wt human pancreatic GH-releasing hormone 1-44 (hpGHRH 1-44) in 33 patients with type I diabetes mellitus, 31 patients with type II diabetes mellitus, and 2 control groups (N = 11 and 8). Based on the results of fundoscopy and fluorescein angiography, the diabetic patients were subdivided into patients without diabetic retinopathy, patients with nonproliferative diabetic retinopathy, and patients with proliferative diabetic retinopathy. Growth hormone responses to hpGHRH 1-44 in diabetic patients with proliferative or nonproliferative retinopathy or without retinopathy were not significantly different regardless of the type of diabetes. Remarkably, GH responses to hpGHRH 1-44 in type I diabetic patients without retinopathy were significantly higher than the matched controls. Our data suggest that diabetic retinopathy in type I and in type II diabetes is not associated with increased GH responsiveness to hpGHRH 1-44, whereas in type I diabetes mellitus without diabetic retinopathy, a GH hyperresponsiveness to hpGHRH seems to occur.
 ...
PMID:No evidence for increased growth hormone responses to growth hormone-releasing hormone in patients with diabetic retinopathy. 310 Mar 67

Growth hormone levels following an intravenous bolus injection of 1 micrograms/kg body weight growth hormone releasing hormone were measured in 21 non-obese and 26 obese patients with Type 2 (non-insulin-dependent) diabetes mellitus and in 13 control subjects. Growth hormone responses in non-obese Type 2 diabetic patients were not statistically different from control subjects. However, obese Type 2 diabetic patients had significantly decreased growth hormone responses to growth hormone releasing hormone when compared with non-obese Type 2 diabetic patients (p less than 0.02). In 9 Type 2 diabetic patients growth hormone releasing hormone tests were performed both during hyperglycaemia and after metabolic improvement by insulin treatment. Growth hormone responses before and after insulin treatment were not statistically different. Our data demonstrate that growth hormone responses to growth hormone releasing hormone in non-obese Type 2 diabetic patients do not differ significantly from control subjects; obesity blunts growth hormone responses to growth hormone releasing hormone in Type 2 diabetes mellitus; and growth hormone responses following growth hormone releasing hormone administration in Type 2 diabetes mellitus are not influenced by the state of metabolic control.
 ...
PMID:Effect of growth hormone releasing hormone on growth hormone secretion in type 2 (non-insulin-dependent) diabetes mellitus. 310 23

The responses of plasma growth hormone-releasing hormone (GHRH) and growth hormone (GH) to oral administration of L-dopa were studied in normal subjects and patients with various endocrine and metabolic diseases to clarify the pathophysiological role of the GHRH-GH axis. In normal subjects, the plasma GHRH concentration was increased from the basal value of 9.8 +/- 1.4 pg/ml (mean +/- SE) to 34.8 +/- 3.1 pg/ml at 30 approximately 90 min after oral administration of 500 mg L-dopa, followed by a rise of GH release (plasma GH level from less than 1 ng/ml to 21.7 +/- 4.7 ng/ml) in most cases, indicating that L-dopa stimulates GH secretion via hypothalamic GHRH. On L-dopa administration, no apparent increases in both plasma GHRH and GH concentrations were observed in patients with hypothalamic hypopituitarism, whereas GHRH administration induced almost normal GH response. In patients with acromegaly, the plasma levels of GHRH remained stationary after the L-dopa administration and did not correlate with plasma GH levels. In subjects with simple obesity, the responses of plasma GHRH (peak 13.2 +/- 1.2 pg/ml) and GH (peak 4.3 +/- 1.7 ng/ml) to L-dopa were significantly lower than those in normal subjects (p less than 0.01). In patients with primary hypothyroidism, peak levels of plasma GHRH (12.6 +/- 1.3 pg/ml) and GH (2.4 +/- 0.6 ng/ml) were significantly lower than those in normal subjects (p less than 0.01). In patients with non-insulin dependent diabetes mellitus (NIDDM), the responses of GHRH and GH were divided into 2 groups; in the responder the peak values of GHRH and GH were 19.4 +/- 8.6 pg/ml and 12.2 +/- 1.4 ng/ml and in the low or non responder 14.7 +/- 1.5 pg/ml and 2.0 +/- 0.6 ng/ml, respectively. Between both groups, there was a significant difference in the values of fasting blood sugar and HbA1 and mean suffering period. These findings suggest that GH secretion evoked by the L-dopa administration is induced by GHRH released from the hypothalamus, and impairment of GH secretion associated with simple obesity, primary hypothyroidism, or NIDDM may be in part attributed to insufficiency of GHRH release from the hypothalamus, and indicate that L-dopa test is clinically useful for evaluating the ability of intrinsic GHRH release in such diseased states.
 ...
PMID:[Effect of oral administration of L-dopa on the plasma levels of growth hormone-releasing hormone (GHRH) in normal subjects and patients with various endocrine and metabolic diseases]. 312 83

A single-blind, randomized, comparative evaluation of glyburide (GL) and chlorpropamide (CP) therapy was performed in twenty previously untreated patients with non-insulin dependent diabetes mellitus (NIDDM) of about two years duration. Only newly diagnosed patients who were never treated and whose fasting blood glucose (FBS) levels were greater than 140 mg/dl after a six to eight week trial of dietary restriction were evaluated. Metabolic studies were performed before and after four months of therapy. GL and CP produced essentially the same effects on serum levels of glucose, insulin, glucagon (IRG), growth hormone (GH), cholesterol, and triglyceride. The mean 24-hour glucose levels for both the GL and CP groups were significantly lower than the pretherapy values (p less than 0.001). The mean 24-hour insulin levels did not change significantly during therapy (p greater than 0.05). Excellent control of plasma glucose was possible during the entire day without producing nocturnal hypoglycemia. Neither GL nor CP therapy influenced the mean 24-hour levels of IRG, GH, or cholesterol. However, mean 24-hour levels of triglyceride were lower in both groups. IRG levels were elevated and the pattern of change in the insulin and IRG levels paralleled each other, which suggested that glucagon may play a role in the resistance of insulin action in NIDDM. GH levels were normal and remained unchanged during therapy. It was concluded that detailed 24-hour studies are important for better understanding the spectrum of abnormalities in newly diagnosed patients with NIDDM who were never treated.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:The 24-hour effects of glyburide and chlorpropamide after chronic treatment of type II diabetic patients. 392 33

The high proportion of unrefined carbohydrates (maize meal) in the diet of Africans could be responsible for their low insulin secretion. The consequent insulinopenia in the general African population may explain the comparative rarity of typical non-insulin dependent diabetes mellitus, and also the virtual absence of coronary heart disease. Changes in growth hormone secretion and in serum lipids, known to be associated with diabetes in Europeans, are also found in African patients.
 ...
PMID:Insulinopenic diabetes in Africa. 469 32

To ascertain whether the dawn phenomenon occurs in nondiabetic individuals and, if so, whether it is due to an increase in glucose production or a decrease in glucose utilization, we determined plasma concentrations of glucose, insulin, C-peptide, and counterregulatory hormones, as well as rates of glucose production, glucose utilization, and insulin secretion at one-half-hourly intervals between 1:00 and 9:00 a.m. in eight normal volunteers. After 5:30 a.m., plasma glucose, insulin, and C-peptide concentrations all increased significantly; rates of glucose production, glucose utilization, and insulin secretion also increased (all P less than 0.05). Plasma cortisol, epinephrine, and norepinephrine increased significantly from nocturnal nadirs between 4:00 and 6:30 a.m. Plasma growth hormone, which had increased episodically between 1:00 and 4:30 a.m., decreased thereafter nearly 50% (P less than 0.05). Plasma glucagon did not change significantly throughout the period of observation. These results indicate that a dawn-like phenomenon, initiated by an increase in glucose production, occurs in nondiabetic individuals. Thus, early morning increases in plasma glucose concentrations and insulin requirements observed in IDDM and NIDDM may be an exaggeration of a physiologic circadian variation in hepatic insulin sensitivity induced by antecedent changes in catecholamine and/or growth hormone secretion.
 ...
PMID:Demonstration of a dawn phenomenon in normal human volunteers. 638 30

Excessive growth hormone (GH) secretion and platelet hyperaggregation have been considered to be involved in the development of the vascular complications of diabetes mellitus (DM). Trying to find a common link between GH and platelet hyperaggregation, we measured von Willebrand or ristocetin cofactor activity (VIII R:Rcof), factor VIII-related antigen (VIII R:Ag) and factor VIII coagulant activity (VIII:C) in ten type 2 DM (NIDDM) and seven normal control (C) human subjects. These three parameters were measured before (time 0), and after a one-hour intravenous infusion of 0.1 U/kg bw of GH, (times 1, 4, 6, and 24 hours). The NIDDM subjects were nonobese and without clinical evidence of diabetic vascular complications. Despite remarkably high levels of GH reached during the infusion (average 280 ng/ml), there were no significant changes in the measured parameters in either NIDDM or C group. The baseline levels of factors VIII R:Rcof, VIII R:Ag and VIII:C were also not significantly different in the two groups. Changes in GH serum levels seem to have no effect on the factors VIII:C, VIII R:Ag or VIII R:Rcof levels in normals (C) or in NIDDM subjects without evidence of vascular complications. These results do not preclude the possibility that there may be a different response to GH in DM patients with advanced vascular complications and probable endothelial cell abnormalities.
 ...
PMID:Lack of von Willebrand factor, factor VIII related antigen and factor VIII coagulant response to human growth hormone infusion in type 2 diabetes mellitus. 642 71

The suggestion of a role for the abnormally regulated growth hormone (GH) in the pathogenesis of diabetes mellitus (DM), implicates also the somatomedins, as mediators of some of GH actions. The present study was aimed at assessing the somatomedin response to exogenous GH administration in diabetes type II (NIDDM) subjects as well as its possible relationship with the degree of control of diabetes. Twenty-two subjects (seven controls and 15 NIDDM patients), matched for sex and age, underwent human GH infusion (0.1 U/kg b.w.) over a one-hour period (time 0 to 1 hour). Total somatomedins (SMs) were measured by human placental membrane radioreceptor assay (in which all SMs crossreact) and Somatomedin-C (SM-C) was determined by a specific RIA. Values were obtained from plasma samples at times 0, 1, 4, 6, and 24 hours. Glycosylated hemoglobin (HbA1a-c) measurements were done from blood samples obtained at time 0. The increase in SMs following GH infusion in NIDDM group was not significantly different from that of the controls. In contrast, the SM-C increase at time 6 and 24 hours were significantly higher than in controls (p less than 0.05 and p less than 0.01, respectively). No significant difference was found between SMs or SM-C response to GH infusion in patients with HbA1a-c greater than 10% vs. less than 10%. These results indicate an exaggerated and prolonged increase in SM-C synthesis following exogenous GH infusion in NIDDM subjects, apparently unrelated to the degree of control of diabetes.
 ...
PMID:Exaggerated somatomedin-C response to human growth hormone infusion in patients with type II diabetes mellitus. 653 51

To investigate whether acute endogenous hyperprolactinemia (h-PRL) influences glucose tolerance in humans, two intravenous glucose tolerance tests were performed in healthy subjects and in patients with untreated type 2 diabetes. One of the tests was carried out during h-PRL induced by oral priming with 10 mg metoclopramide (MET). The other was performed during normoprolactinemia (n-PRL) prevailing after oral priming with placebo. The glucose disappearance rates (Kg) were compared in the n-PRL and h-PRL states. In eight healthy subjects with high Kg values (greater than or equal to 1.2) during n-PRL, the glucose tolerance decreased during MET-induced h-PRL. This was reflected by a Kg fall from 2.0 +/- 0.4 during n-PRL to 1.3 +/- 0.3 during h-PRL (P less than 0.01). It is unlikely that this Kg decline could have been caused by prolactin-induced changes in serum levels of insulin, cortisol, or growth hormone (GH), since these hormones showed glucose-elicited response patterns that were similar in the n-PRL and h-PRL states. It is also improbable that MET per se could have caused Kg to fall, inasmuch as MET left Kg unaffected when oral pretreatment with bromocriptine prevented MET from inducing h-PRL in an additional five healthy subjects with high Kg values.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Does acute endogenous hyperprolactinemia affect intravenous glucose tolerance in humans? 672 56


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>