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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 effect of antisomatotropin serum (ASS), raised in horse against human growth hormone, on the carbohydrate metabolism of diabetics has been investigated. Among the eight diabetic patients treated so far two had GH secreting pituitary adenoma, two insulin-dependent, and four others adult onset diabetes mellitus. The glucose tolerance curve improved in all but one patient. The effect lasted for two--four weeks. Because of this short time of efficiency, the place of ASS in the definite treatment of diabetes mellitus cannot been judged so far, however, its administration in diabetic retinopathy seems to be advantageous.
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PMID:Administration of antisomatotropin serum in diabetes mellitus. 722 26

Exaggerated growth hormone (GH) responses to various provocative stimuli have been reported previously in insulin-dependent diabetes mellitus (IDDM). Little is known about GH response to synthetic gonadotropin-releasing hormone (GnRH) in diabetes. It has been reported to be exaggerated in active acromegaly. We investigated GH, follicle-stimulating hormone (FSH) and luteinizing hormone (LH) levels after GnRH administration in seven IDDM and eight non-insulin-dependent diabetic (NIDDM) patients. They were poorly controlled from a metabolic point of view. Ten healthy subjects served as the control group. FSH and LH levels increased significantly after GnRH in all groups. In contrast, GnRH did not elicit significant GH increments above baseline levels in any group. Moreover, mean areas under the GH curves were comparable among the three groups. These results suggest that poorly controlled IDDM and NIDDM does not lead to inappropriate GH responses to GnRH.
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PMID:Does gonadotropin-releasing hormone administration affect serum growth hormone levels in poorly controlled insulin-dependent and non-insulin-dependent diabetes mellitus? 759 3

Because of its multi-faceted potential as a neurotrophic factor, insulin-like growth factor I (IGF-I) has been given to hundreds of ALS patients world-wide. Unlike some patients with post-polio syndrome and fragile elderly males, it is unclear whether any of these patients possess disturbances in IGF signaling. We found that about 25% of ALS patients in a controlled trial of human growth hormone (hGH) had lower or higher than normal IGF-I serum levels. Many ALS patients do have some of the characteristics of type II diabetes mellitus, where IGF-I therapy is also under way. In addition, in type I diabetes significant increase in a circulating molecule that binds IGF-I, IGF-I binding protein 1 (IGFBP-1), occurs along with reduced IGF-I, when neuropathic complications are prominent. We have studied the response of IGFBPs in ALS patients to subcutaneous rhIGF-I and found transient induction of IGFBP-1. Studies related to the IGFBPs have not been done in familial ALS (FALS) patients. However, the gene for another IGFBP, BP-2, co-localizes with the gene for juvenile ALS (ALSJ) on chromosome 2. IGF-I has been given to several models of motor neuron degeneration in the mouse, including motor neuron disease and wobbler, with beneficial effects. However, it is also not known whether any accepted genetic mouse model of motor neuron degeneration possesses any disturbance in the IGF signaling system.
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PMID:The insulin-like growth factor signaling system and ALS neurotrophic factor treatment strategies. 759 1

We have compared intraoperative glycaemic control, insulin requirements and metabolic and endocrine variables in 40 non-insulin-dependent diabetic patients (NIDDM) and 40 insulin-dependent diabetic patients (IDDM) undergoing general anaesthesia for elective procedures. Two i.v. insulin regimens were used: continuous i.v. infusion (group A: 1.25 u.h-1) and repeated i.v. boluses (10 u./2 h). Blood concentrations of glucose were measured every 15 min from just before induction of anaesthesia until 2 h after surgery. Plasma lactate and pyruvate concentrations, ketone bodies, C-peptide and counter-regulatory hormones were also measured. Glycaemia did not differ significantly in the two types of diabetes, regardless of the insulin therapy used. The amounts of insulin administered were similar in NIDDM and IDDM. There was no significant difference for other metabolic variables. Plasma concentrations of growth hormone (GH) increased significantly during surgery, especially in IDDM patients, but this change did not alter intraoperative glycaemic control. We conclude that mean glycaemic control, insulin requirements and development of ketone bodies in NIDDM and IDDM patients did not differ during the operative period, regardless of the insulin regimen used. Therefore, during the operative period, it is not necessary to modify the insulin regimen according to the type of diabetes. The consequences of increased plasma GH concentrations on glycaemic control in IDDM patients after operation are unknown.
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PMID:Intraoperative glycaemic control in non-insulin-dependent and insulin-dependent diabetes. 799 82

A suppressed growth hormone (GH) response to GH-releasing hormone (GHRH) in both lean and overweight type II diabetics has been reported. Pyridostigmine (PD), an acetylcholinesterase inhibitor, elicits GH secretion when administered alone and enhances the GH response to GHRH in normal subjects. The aim of our study was to evaluate the effect of PD on GHRH-stimulated GH secretion in both lean and obese type II diabetic patients. We studied 16 patients with type II diabetes mellitus (seven lean and nine obese). Eleven nondiabetic subjects (six lean and five obese) served as controls. Each subjects underwent treatment with (1) 120 mg PD orally or (2) 2 tablets of placebo orally, 60 minutes before intravenous (IV) injection of 100 micrograms GHRH-(1-29)NH2. We have found no significant differences in GH responses to GHRH between obese diabetics and obese controls. On the other hand, the absolute GH levels were significantly suppressed in lean type II diabetics compared with lean controls at 15 and 30 minutes after GHRH injection. Obese diabetic subjects had slightly but not significantly decreased GH responses to GHRH+PD compared with obese nondiabetic subjects (8.36 +/- 1.62 v 14.4 +/- 7.62 micrograms/L). Lean type II diabetics showed a blunted GH release after GHRH+PD compared with normal-weight healthy subjects (GH peaks, 15.77 +/- 2.17 v 40.88 +/- 6.17 micrograms/L, P < .05). PD enhanced significantly the GH response to GHRH in obese diabetics, obese controls, and non-obese controls (P < .05), but not in non-obese type II diabetics.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of pyridostigmine on the growth hormone response to growth hormone-releasing hormone in lean and obese type II Diabetic patients. 802 15

Growth hormone secretion is blunted in obesity. Recent studies have shown that the sub-group of obesity with preponderance of accumulation of fat in visceral depots is associated with endocrine abnormalities. We therefore measured IGF-I concentrations in serum in 27 men who also underwent computerized tomography measurements of regional and total body fat mass. Furthermore, euglycemic-hyperinsulinemic glucose clamps were used to determine insulin resistance, and established 'risk factors' for cardiovascular disease and non-insulin dependent diabetes mellitus were measured, i.e. blood pressure, plasma lipids, and blood glucose, as well as sex steroid hormones. Visceral fat mass systolic blood pressure and triglycerides were higher (P < 0.05) in the group with low (87 +/- 4 micrograms/l) IGF-I values, compared to those with high (126 +/- 6 micrograms/l) IGF-I values, divided after the median value. IGF-I was negatively correlated with visceral fat mass (r = 0.40), independently of subcutaneous and total fat mass. As described before visceral fat mass was directly associated to a majority of the measured 'risk factors', as well as indirectly to testosterone and sex hormone binding globulin (SHBG) concentrations. The latter were also strongly related statistically to the 'risk factors'. IGF-I concentrations showed, however, weaker correlations with the metabolic factors, blood pressure or sex steroid hormones. Multivariate analyses revealed that the correlations of visceral fat with the risk factors were not influenced by IGF-I, while testosterone or SHBG totally abolished these associations. The results indicate that low serum IGF-I concentrations, suggesting deficient growth hormone secretion, are associated with visceral but not with subcutaneous or total fat masses.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Low concentrations of insulin-like growth factor-I in abdominal obesity. 838 69

Several endocrine insufficiencies develop with aging. These not only include the sex steroid hormones in both sexes, but probably also growth hormone. These hormonal systems apparently interact at central and peripheral levels. Deficiencies seem to result in altered body composition, with more body fat, particularly in central depots, combined with a decreased muscle mass. In addition, risk factors for cardiovascular disease and non-insulin dependent diabetes mellitus accumulate concomitantly. Intervention studies now begin to show that this is at least partly reversible with appropriate substitution. Nutritional deficiencies with aging may be coupled to these endocrine insufficiencies, perhaps mediated via psychological factors and loss of energy, which are also associated with the body alterations. If these deficiencies can be successfully corrected, then part of the nutritional problem of aging people may well develop into a more organizational, psychosocial and political type of problem.
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PMID:Endocrine insufficiency and nutrition in aging. 839 47

Blood levels of intermediary metabolites were measured and indirect calorimetry was performed in 10 otherwise healthy, non-insulin-dependent diabetic (NIDDM) patients before, during, and after 30 minutes of moderate exercise on three occasions in random order at weekly intervals with (1) heparin treatment to increase preexercise plasma nonesterified fatty acid (NEFA) levels (HEPARIN); (2) acipimox, a nicotinic acid analogue, to reduce preexercise plasma NEFA levels (ACIPIMOX); and (3) no manipulation of preexercise plasma NEFA levels (NIL). With ACIPIMOX, preexercise blood levels were significantly reduced for NEFAs and glycerol (P < .01) and marginally reduced for acetoacetate and 3-hydroxybutyrate (NS) compared with preexercise levels for the other two treatments; these low levels seen with acipimox treatment increased only slightly during exercise and the postexercise period. Plasma NEFA levels increased by approximately 150% (P < .001) with HEPARIN at the same times. The levels of ketone bodies during either NIL or HEPARIN increased rapidly postexercise by approximately 90% to 110% for both acetoacetate and 3-hydroxybutyrate (both P < .01). Plasma insulin levels tended to be lowest (despite similar plasma glucose levels during the three treatments) with ACIPIMOX, while growth hormone (hGH) and, perhaps, noradrenaline levels were highest both during and after exercise. The respiratory quotient (RQ) was highest with ACIPIMOX (P < .05 for exercise and postexercise periods compared with the other two treatments), which, compared with NIL, reduced fat oxidation by 27% and 60% and increased carbohydrate oxidation by 29% and 74% during and after exercise, respectively (all P < .05). These changes in substrate oxidation due to ACIPIMOX were almost opposite to those observed with HEPARIN.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effects of changes in plasma nonesterified fatty acid levels on oxidative metabolism during moderate exercise in patients with non-insulin-dependent diabetes mellitus. 848 64

Diurnal variation in insulin sensitivity in patients with NIDDM has long been suspected but has been difficult to document mainly because of the interdependence of changes in glucose and insulin. Stable serum insulin levels during hyperglycemic clamping in patients with NIDDM in the present study provided the opportunity to examine changes in insulin sensitivity unaffected by changes in blood glucose and insulin concentrations. Six patients with NIDDM (four men and two women, BMI 33.9 +/- 2.5) underwent hyperglycemic (11.1 mmol/l, approximately 200 mg/dl) clamping for 72 h. Measured were serum insulin, free fatty acid (FFA), cortisol, and growth hormone concentrations and rates of insulin secretion, insulin clearance, and glucose infusion rate (GIR) needed to maintain hyperglycemia. In addition, five patients (three men and two women, BMI 32.6 +/- 0.6) underwent hyperglycemic clamping for 24 h with hourly determinations of hepatic glucose production (HGP) and glucose disappearance rates (GRd). GIR, reflecting insulin sensitivity, changed rhythmically with a cycle duration of 22.9 +/- 1.4 h and an amplitude of 47.8 +/- 11.2%. GIR was lowest at 8:31 a.m. (+/- 52 min) and highest at 7:04 p.m. (+/- 58 min). Circadian changes in GIR were completely accounted for by changes in HGP, while GRd remained unchanged. Plasma levels of FFAs and cortisol also exhibited circadian fluctuations, and their blood levels correlated negatively with GIR (r = -0.72 and -0.64, respectively). We concluded that insulin sensitivity in patients with NIDDM changed with circadian (approximately 24 h) rhythmicity (decreasing during the night and increasing during the day). These changes were unrelated to blood levels of glucose and insulin, insulin clearance, exercise, food intake, and sleep. They were caused by circadian changes in HGP, which in turn were closely correlated with circadian changes in blood FFA and cortisol levels. We believe that recognition of these circadian changes has implications for the diagnosis and the treatment of patients with NIDDM.
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PMID:Evidence for a circadian rhythm of insulin sensitivity in patients with NIDDM caused by cyclic changes in hepatic glucose production. 869 Jan 50

We conducted a randomized, prospective study to assess the effect of i.v. insulin on blood glucose control, development of ketone bodies and hormonal changes in 60 well-controlled, non-insulin-dependent diabetics (NIDDM) undergoing major surgery. In group A, patients were given only 0.9% saline; in group B, patients were given insulin as a continuous i.v. infusion (1.25 u. h-1); in group C, patients were given insulin 10 u. i.v. boluses every 2 h. Patients in all three groups were given insulin 5 u. when their intraoperative blood glucose concentration increased to greater than 11.1 mmol litre-1. Blood glucose concentrations were measured every 15 min, from just before induction of anaesthesia to 2 h after surgery. Plasma lactate, pyruvate, ketone body, C-peptide and counter-regulatory hormone concentrations were also measured. Blood glucose concentrations in the three groups did not differ significantly. There was a mild-to-moderate increase in plasma ketone body concentrations in group A, but without any deleterious consequences. Plasma C-peptide concentrations decreased significantly in groups B and C, especially in patients given bolus injections of insulin. Plasma growth hormone concentrations also increased significantly in group B and C patients. This study indicated that the "no insulin--no glucose" regimen was a simple, effective way to control blood glucose in well-controlled NIDDM patients, provided blood glucose was measured frequently and insulin used appropriately.
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PMID:Use of i.v. insulin in well-controlled non-insulin-dependent diabetics undergoing major surgery. 877 97


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