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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To assess the role of insulin resistance and insulin deficiency in the pathogenesis of diabetic retinopathy in non-insulin-dependent diabetes mellitus, 13 patients with and 12 patients without retinopathy were studied. The glucose clamp technique was used to measure insulin resistance and insulin response to glucose. During the euglycemic clamp, at comparable steady-state levels of glucose and insulin, the mean glucose infusion rate, which indicates the rate of glucose utilization, was lower in the retinopathy group than in the nonretinopathy group (6.1 +/- 0.5 versus 8.1 +/- 0.7 mg . kg-1 . min-1, P less than 0.02). Growth hormone (GH) concentrations were higher in the retinopathy group 8.4 +/- 2.5 versus 2.5 +/- 0.7 microIU/ml, P less than 0.05), but they did not correlate significantly with insulin resistance, expressed as mean glucose turnover. During the hyperglycemic clamp (+7 mmol/L above the fasting plasma glucose), the insulin response in the two groups of diabetics was similar. Increased insulin resistance represents an additional factor, which together with other factors, may be important in the pathogenesis of diabetic microvascular complications.
Diabetes 1983 Jan
PMID:Insulin resistance and insulin deficiency in diabetic retinopathy of non-insulin-dependent diabetes. 633 6

In insulin-dependent diabetics, insulin requirements increase significantly after 0600 h, resulting in prebreakfast hyperglycemia with either conventional insulin therapy or constant insulin infusions with insulin infusion devices. In order to clarify the role of the pituitary-adrenocortical axis and further examine the mechanisms of the phenomenon of nocturnal variability in insulin requirements, we studied five IDDs using a closed-loop insulin infusion device (Biostator, GCIIS). The subjects were given saline (SAL) or dexamethasone (DEX) i.v. from 1800 to 0900 h on successive nights. From 2400-0300 to 0600-0900 h, mean insulin infusion rates required to maintain blood glucose values between 109 and 120 mg/dl increased by 0.21 +/- 0.05 mU/kg/min during the SAL infusion, and 0.16 +/- 0.04 mU/kg/min during the DEX infusion, when plasma cortisols were suppressed to less than or equal to 2 micrograms/dl. Mean free insulin concentrations did not increase and remained constant throughout both study nights in spite of the significantly higher 0600-0900-h insulin infusion rates. Growth hormone, glucagon, epinephrine, and norepinephrine concentrations showed normal nocturnal and early morning patterns during both study nights. We conclude that the nocturnal variability in insulin requirements persists despite suppression of the pituitary-adrenocortical axis, and that increased free insulin clearance or degradation may contribute to the "dawn phenomenon" of rising prebreakfast glucose despite constant insulin infusion.
Diabetes 1983 May
PMID:Examination of the role of the pituitary-adrenocortical axis, counterregulatory hormones, and insulin clearance in variable nocturnal insulin requirements in insulin-dependent diabetes. 634 Nov 22

We have evaluated the endocrine changes in 10 male subjects with hemochromatosis. Two subjects initially had aplastic anemia, and the remainder had idiopathic hemochromatosis. Four of the ten patients had diabetes mellitus. Sexual dysfunction (impotence and/or decreased libido) was observed in 8 subjects. Six patients had subnormal testosterone levels; FSH levels were almost uniformly low, but LH concentrations were more variable. Only three patients had normal testosterone responses to hCG. Hypothyroidism, free T4 less than 0.9 ng/dl, was present in 4 subjects, and the etiology was heterogeneous. Basal prolactin levels were elevated in 2 patients and failed to respond adequately to TRH in 2 other patients. Growth hormone reserve was normal in all but 1 patient, and pituitary-adrenal reserve was normal in all but 1 patient. We conclude that disturbances in both pituitary and end-organ function are observed in hemochromatosis. These central and end-organ defects may exist alone or simultaneously. Hypogonadism is almost universal, and is a consequence of defective function of the hypothalamic-pituitary axis and/or primary Leydig cell disturbance. Other evidence of pituitary disturbance are observed but are rather uncommon.
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PMID:The endocrine manifestations of hemochromatosis. 634 90

Elevated plasma concentrations of growth hormone impair glucose tolerance and insulin sensitivity of peripheral tissues. To study the effect of short-term exposure to growth hormone concentrations elevated into the upper physiologic range (7-10 ng/ml) on splanchnic carbohydrate metabolism, both splanchnic glucose output (SGO) and substrate exchange after ingestion of a 75-g glucose load were determined by means of the liver vein catheter technique in six healthy volunteers after growth hormone administration. Growth hormone was infused at a rate of 2 micrograms/kg X h starting 120 min before and continuing for 150 min following the glucose load. Control studies without growth hormone administration were performed in seven subjects. SGO was 104 +/- 10 (SEM) mg/min in the postabsorptive state and increased to 43.4 +/- 2.2 g during the 150-min period following glucose ingestion. Growth hormone infusion did not alter basal SGO (130 +/- 14 mg/min), nor the splanchnic exchange of lactate, pyruvate, and free fatty acids, whereas basal production of beta-OH-butyrate was increased twofold; following glucose ingestion a higher proportion of the given glucose load escaped the splanchnic bed after growth hormone exposure (66.9 +/- 6.8 g/150 min; P less than 0.005). The insulin production rate (basal 14 +/- 2 mU/min; following oral glucose 7.0 +/- 0.8 U/150 min) as calculated from C-peptide release from the splanchnic area was unaltered by growth hormone exposure in the basal state (14 +/- 3 mU/min), but augmented after glucose ingestion (14.8 +/- 1.5 U/150 min).(ABSTRACT TRUNCATED AT 250 WORDS)
Diabetes 1984 Jan
PMID:The effect of growth hormone on splanchnic glucose and substrate metabolism following oral glucose loading in healthy man. 636 Jul 65

In two girls (14 and 16 years) and one boy (19 years) with PLW-syndrome and pronounced obesity (240, 210 and 77% overweight) endocrine function tests were carried out. Growth hormone secretion was decreased but normalized after reduction of weight. Thyroxin levels as well as basal and TRH stimulated TSH concentrations were normal. HCG application in the boy induced no rise of the normal basal testosterone levels. Oral glucose tolerance test demonstrated an increased stimulation of insulin in two cases, no other symptoms of diabetes mellitus were found. In the LHRH test an insufficient rise of gonadotropins was found. However, after two weeks of pernasal application of an LHRH analogue (D-Leu6-des-Gly10-EA) the gonadotropin stimulation was distinctly improved and onset of puberty was induced in the male patient. These results are indicative of a hypothalamic disturbance in patients with PLW-syndrome.
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PMID:[Endocrine studies on the Prader-Labhart-Willi syndrome: puberty induction in a 19-year-old boy after long-term treatment with an LHRH analog]. 641 33

Growth hormone (GH) response was studied in 8 insulin-dependent and 7 non-insulin-dependent diabetics after stimulation with L-Dopa (500 mg orally) and TRH (0.2 mg iv.). L-Dopa induced a clear GH response in insulin-dependent diabetes (IDDM) and in the control group while in non-insulin-dependent diabetes (NIDDM) peak GH levels were lower (P less than 0.05) and 4 of 7 subjects failed to respond to L-Dopa stimulation. TRH had no effect on GH levels in NIDDM and in the controls. Insulin-dependent diabetics responded to TRH stimulation and GH levels at 20 and 30 min were significantly higher as compared with NIDDM and the control group. The degree of hyperglycemia seemed not to influence GH response. The highest GH levels were noted in two patients with proliferative retinopathy. It is suggested that TRH-induced GH release may be a characteristic feature in some patients with IDDM.
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PMID:TRH-induced growth hormone release in insulin-dependent diabetes mellitus. 644 6

Human insulin (recombinant DNA) and purified pork insulin (PPI) were administered intravenously at a dosage of 0.075 U/kg in eight healthy men. Both insulins exerted the same hypoglycemic effect with the same restoration pattern to normal glucose levels at the end of the test. Differences were found with respect to a stronger antilipolytic and antiketogenic effect of human insulin; also the reactive rise of both compounds at the end of the test is less under human insulin in comparison with PPI. In spite of the same glucose nadir, the pattern of hormonal counterregulation is different under human insulin in comparison with PPI. There was less epinephrine and glucagon and practically no prolactin secretion following human insulin. Growth hormone secretion is augmented under human insulin. The clinical significance of these results under long-term treatment with human insulin has to be assessed.
Diabetes Care
PMID:Comparative studies on intermediary metabolism and hormonal counterregulation following human insulin (recombinant DNA) and purified pork insulin in man. 676 48

Diabetes mellitus was diagnosed in an aged bonnet macaque (Macaca radiata). Six months later the monkey was found comatose. Laboratory findings of extreme hyperglycemia, hyperosmolality, and glycosuria without ketonuria were consistent with a diagnosis of hyperosmolar, non-ketotic diabetic coma (NKC). Further laboratory studies disclosed very low levels of immunoreactive insulin and depressed free fatty acid values. Growth hormone and cortisol levels were within normal limits.
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PMID:Hyperosmolar non-ketotic diabetic coma in the nonhuman primate: a first report. 685 68

In normal fasting dog serum, the insulin: proinsulin molar proportion was 71:29%. In response to glucose infusion, the proinsulin proportion decreased. In the pancreas, the proinsulin proportion was lower than in serum. Growth hormone treatment for one day increased serum insulin sevenfold and proinsulin 18-fold. The proinsulin proportion increased to 49%. The growth hormone injections magnified the response to glucose infusion. The rise in serum insulin was 16 times the normal, proinsulin also rose but its proportion decreased. Growth hormone treatment for 6 days decreased pancreatic insulin to 5% and proinsulin to 46% of normal. In the permanent (metasomatotrophic) diabetes produced by the prolonged administration of growth hormone, serum insulin decreased in the proinsulin proportion increased. No rises in serum insulin nor proinsulin occurred following glucose infusion. In the pancreas, insulin and proinsulin were reduced to 1.6% and 8% of normal. The reduction in the immunoreactive insulin in the pancreas was more pronounced in the tail than in the head and body regions. The results indicate that in the state of augmented insulin secretion and hyperinsulinaemia produced by growth hormone and in the reduced insulin secretion and hypoinsulinaemia of metasomatotrophic diabetes, the proportion of proinsulin in serum is increased due to beta cell secretion containing a higher proportion of proinsulin than normal
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PMID:Growth hormone and metasomatotrophic diabetes: effects on insulin and proinsulin of serum and pancreas in dogs. 704 Jan 45

The large vessel disease develops slowly and progressively among most diabetics. According to the concept of a specific diabetic macroangiopathy, the alterations in the large vessels are part of the general diabetic angiopathy and are different from the spotty atherosclerosis. This hypothesis proposes that the changes develop a consequence of the metabolic situation in diabetes. The concept is based on epidemiologic, clinical, and patho-anatomical observations. A model of large-vessel disease in diabetes is briefly described. Diabetic serum causes proliferation of the aortic myomedial cells in culture. Growth hormone causes a similar proliferation. Type 1 procollagen and fibronectin elaboration is enhanced by diabetic serum. The same effect has been found with growth hormone. Insulin treatment in experimental diabetes prevents the proliferation of arterial myomedial cells in the coronary arteries. The presented data are compatible with the concept of a diabetic macroangiopathy distinct from atherosclerosis.
Diabetes 1981
PMID:Diabetic macroangiopathy and growth hormone. 729 69


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