Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0497406 (overweight)
 26,365 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Tolbutamide (25 mg/kg: maximum 1 mg) intravenously (IV) and glucagon (0.03 mg/kg; maximum 1 mg) intramuscularly (IM) were given sequentially to 12 untreated girls with XO-Turner's syndrome (ages 6.5 to 17.0 years) and to ten female siblings (ages 8.0 to 16.7 years) to evaluate blood sugar (BS), plasma free fatty acids (FFA), serum immunoreactive insulin (IRI), and growth hormone (IRGH) responses to these insulinogenic secretagogues in order to appreciate any differences of genotypes on carbohydrate metabolism within identical family backgrounds. Seven of 12 patients with Turner's syndrome (58%) but none of the siblings were 20% or more overweight for height. There was a family history of diabetes mellitus in 7 to 12 patients (58%). The results showed significant elevations of mean FFA levels and decreased mean IRI responses to both insulinogenic stimuli without differences in mean BS or serum IRGH responses in the Turner's syndrome patients when compared to the controls. Three of 12 patients (25%) had abnormally elevated and prolonged blood sugar responses to IM glucagon. These findings show a significant incidence of abnormal carbohydrate and lipid metabolism and insulin deficiency in untreated patients with XO-Turner's syndrome when compared to normal female siblings and implicate this chromosomal defect in the impaired insulin secretion.
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PMID:Turner's syndrome and carbohydrate metabolism. I. Impaired insulin secretion after tolbutamide and glucagon stimulation tests: evidence of insulin deficiency. 46 42

The efficacy and safety of gliclazide (Diamicron) were studied in 29 NIDDM patients (19 men and 10 women aged 25-68 years) who failed to improve with diet or with diet plus a sulfonylurea. All patients were overweight and had fasting blood glucose levels consistently above 150 mg/dl (8.24 mmol/l). After withdrawal of oral hypoglycemics where applicable, they received 40 mg Diamicron three times daily with meals. The dose was increased by 40-80 mg/day until optimum control was obtained or up to a maximum of 320 mg/day. Treatment lasted for 12 months. At the end of this period the mean fasting blood glucose level had fallen by 35% from 238 to 154 mg/dl and the mean 2-h postprandial blood glucose level had fallen by 28% from 237.7 to 195 mg/dl. The mean glycosylated hemoglobin level also fell by 30% from 10.10 to 7.02%, i.e. within the normal range. In addition, there was a 19% fall in triglyceride and a 10% fall in cholesterol levels, with no change in body weight. No changes were observed for serum insulin, C-peptide and glucagon levels, thyroid function tests, blood counts, liver and kidney function tests, uric acid, electrolytes, blood pressure or heart rate. No clinical or ECG abnormalities were observed in patients with or without cardiovascular disease. There were two presumptive hypoglycemic reactions, but these did not require treatment. Adverse effects were reported by 22 patients, including dizziness and light-headedness, diarrhea, nausea, palpitations and pruritus, but none required modification of Diamicron therapy. The results therefore show that Diamicron is safe, effective and well tolerated in suitably selected NIDDM patients.
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PMID:Evaluation of the efficacy and safety of Diamicron in non-insulin-dependent diabetic patients. 179 70

To investigate the glucagon status of women with polycystic ovary syndrome (PCO) and to relate this to serum concentrations of insulin, androgens and SHBG, 44 women with PCO and 23 control subjects underwent a 75-g oral glucose tolerance test. Although obese (body mass index greater than 30 kg/m2) women with PCO had higher concentrations of glucose and insulin than overweight (BMI 25-30 kg/m2) and non-obese (BMI less than 25 kg/m2) women with PCO and control subjects, fasting and summed values of glucagon in response to oral glucose were similar in all groups. The fasting and summed concentrations of glucagon were inversely related to those of testosterone and androstenedione in obese women with PCO, but no other relationships were demonstrated between hormone values and those of glucagon in the other groups. We conclude that glucagon is not implicated in peripheral insulin resistance in women with PCO.
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PMID:Glucagon in women with polycystic ovary syndrome (PCO): relationship to abnormalities of insulin and androgens. 214 2

The frequency of secondary failure to oral hypoglycaemic agents (OHA) in patients with non-insulin dependent diabetes (NIDDM) is still unknown, despite more than 30 years of use of OHA. The term secondary failure should be limited to patients who, despite maximal dosages of OHA and despite full compliance with diet and therapy, are no longer controlled and require insulin to obtain an acceptable glucose metabolism. We evaluated 248 out-patients, either on OHA, or on insulin because of poor metabolic control with OHA, in order to assess duration of treatment with OHA since diagnosis, by means of actuarial curves (Mantel-Cox test). Patients with low relative body weight (RBW less than or equal to 100) experienced secondary failure earlier and more often than obese patients (RBW greater than 120) or overweight (RBW 101-120) patients. In 66 of the above out-patients, 33 OHA-treated and 33 insulin-treated, matched for age at onset and duration of disease, islet-cell-antibodies (ICA) and C-peptide release at fasting, 6 min after i.v. glucagon and post prandially were evaluated. Only among lean and overweight patients, was C-peptide release significantly lower in insulin-treated than in OHA-treated patients; differences disappeared in obese patients. ICA were found in only 7 patients (10.6%). HLA phenotype was different from that of healthy blood donors for the loci HLA B5, B13, CW4, with no differences between OHA-treated and insulin-treated patients. These data indicate that secondary failure is more frequent in lean patients with NIDDM, and is related to reduced insulin release.
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PMID:Secondary failure to oral hypoglycaemic agents in non-obese patients with non-insulin-dependent diabetes is related to reduced insulin release. 266 Dec 81

Hypertension in diabetic patients is more common than in controls, contributes substantially to their increased cardiovascular morbidity and mortality, and should be treated as accurately as diabetes mellitus itself. After appropriate exclusion of secondary forms, the first therapeutic step consists of reduction of overweight, salt intake, and smoking; the omission of interfering drugs; and adequate instruction. Step 2 has usually been the prescription of a diuretic drug, in spite of its known side effects on carbohydrate and lipid metabolism. A new possible alternative may be a calcium antagonist. Results in 10 hypertensive diabetic persons suggest that at a dose that normalizes blood pressure, neither carbohydrate nor lipid metabolism is altered, uric acid decreases, the exaggerated cardiovascular reactivity toward norepinephrine becomes normal, and the pressor dose for angiotensin II tends to rise. Body weight, blood volume, exchangeable sodium, as well as plasma and urinary sodium, potassium, and creatinine levels were unchanged. The third therapeutic step is the addition of a cardioselective beta blocker in a moderate dose. This avoids the disadvantages of beta 2-adrenergic blockade such as decreased insulin output, prolonged hypoglycemia, diminished glucagon secretion, and increased vasospasticity during hypoglycemic states, as well as aggravation of peripheral vascular disease. Alternatives are other sympatholytics with their known tendency to cause or increase orthostatic and sexual problems or, again, a calcium antagonist. In step 4, a hydralazine-type drug or prazosine is added. The fifth step, which adds minoxidil or captopril to the previous drugs, should only be taken after a specialist reevaluates the overall situation.
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PMID:Antihypertensive therapy in diabetic patients. 286 38

We performed a double-blind crossover trial of challenges with 30 mg of aspartame per kilogram of body weight or placebo in 40 subjects who reported having headaches repeatedly after consuming products containing aspartame. The incidence rate of headache after aspartame (35 percent) was not significantly different from that after placebo (45 percent) (P less than 0.50). No serious reactions were observed, and the incidence of symptoms other than headache following aspartame was also equivalent to that after placebo. No treatment-related effects were detected in vital signs, blood pressure, or plasma concentrations of cortisol, insulin, glucagon, histamine, epinephrine, or norepinephrine. Most of the subjects were well educated and overweight and had a family or personal history of allergic reactions. The subjects who had headaches had lower plasma concentrations of norepinephrine (P less than 0.0002) and epinephrine (P less than 0.02) just before the development of headache. We conclude that in this population, aspartame is no more likely to produce headache than placebo.
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PMID:Aspartame and susceptibility to headache. 365 89

Glucose tolerance is impaired in normal pregnancy and in approximately 1% of all pregnant women gestational diabetes develop. The present paper reviews the pathogenesis of these changes based on the modifications of glucagon and insulin secretion and action. Fasting plasma glucagon levels are increased in pregnancy in normal and gestational diabetic women. After glucose ingestion or infusion the suppression of glucagon levels is enhanced in pregnancy whereas the response to protein is unaffected. The results indicate that the changes in glucagon secretion in pregnancy are secondary to altered plasma glucose levels. In all women the fasting plasma insulin levels and the glucose--or protein--induced insulin response is increased in pregnancy. The responses are similar in normal women and normal weight gestational diabetics whereas greater responses are seen in overweight gestational diabetics. Morphological and physiological animal studies demonstrate B-cell hypertrophy and hyperplasia and increased insulin secretory responsiveness in pregnancy, which is corroborated by human studies showing an almost 4-fold increase in insulin response when the same glycemic stimulus is applied in pregnancy and postpartum. The increased insulin responsiveness seems to be caused by pregnancy-related changes in the secretion of progesterone, estradiol, human placental lactogen (hPL) and prolactin. However, the increased insulin levels are unable to maintain normal glucose tolerance and pregnancy, thus, is a state of insulin resistance. Receptor studies yield diverging results, but indicate a postreceptor defect in insulin action in pregnancy. This may be caused by the increased cortisol levels in pregnancy, as significant positive correlations between increases in cortisol levels and the decreases in glucose tolerance have been established in normal pregnant women.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:On the decrease of glucose tolerance in pregnancy. A review. 390 79

One group of 10 obese people (1.72 times normal weight) was compared to a control group of 9 normal-weight subjects. Oxygen consumption (VO2), immuno reactive growth hormone (IRGH), and rectal temperature (Tre) were measured every 15 min on an average, during the 5 h following a protein meal composed of 6 egg-whites and 50 g of casein totaling 1 340 kJ. The results show that postprandial thermogenesis (PPT) is the same in both groups: maximum increase in VO2 averages 15% in the obese and 16% in the control groups respectively. Energy expenditure integrated over the 5 h was 129 kJ for the obese and 114 kJ for the control subjects, i.e. 9.6% and 8.5% of the energy meal content. The rise in Tre was identical for both groups (0.4 degrees C over 3 h). For IRGH, the preprandial reference figures were much lower in the obese: 52 pmole.dm-3, as compared to 145 pmole.dm-3. In all control subjects, the protein meal resulted in a IRGH peak of, on average, 455 pmole.dm-3 about 2 h after. This was not observed in 4 of the obese subjects, while in the remaining 6, the mean peak value was 165 pmole.dm-3, occurring after 1 h. The other hormonal or chemical compound simultaneously analysed (glucagon, cortisol, PRL, T3, glucose, lactate, NEFA) do not show any significant variations but insulin blood level for which a postprandial increase was measured in both groups. It is concluded that after a protein test meal: PPT in overweight people is no different from that in people of normal weight.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Postprandial thermogenesis and hormonal release in lean and obese subjects. 391 63

The effect of antihypertensive therapy with guanabenz or hydrochlorothiazide (HCTZ) on the secretion of growth hormone, prolactin, insulin, and glucagon was evaluated in double-blind fashion in 45 patients. Fifteen patients were treated with HCTZ, 50 mg twice daily, and 30 patients were treated with twice-daily dosages of guanabenz ranging from 4 to 32 mg. Blood samples for hormone analysis were collected during maintenance therapy when blood pressure was controlled as well as 1 week after the withdrawal of the antihypertensive medications. Serum levels of growth hormone and prolactin were within the normal ranges and were unchanged during treatment with HCTZ or guanabenz at any dose level. Interpatient variability in insulin levels was high, although within-subject insulin levels generally were consistent. No treatment effects were seen for insulin levels among guanabenz- or HCTZ-treated patients. Glucagon levels generally were above the expected range for fasting patients and were lower in patients receiving 4 or 8 mg of guanabenz twice daily than in those receiving 16 mg twice daily (p less than 0.05) and in those treated with HCTZ (p less than 0.01). However, analysis of paired data revealed no changes in glucagon levels upon withdrawal of guanabenz, whereas glucagon levels were higher during HCTZ treatment than after drug withdrawal (p = 0.012). Since guanabenz treatment did not affect the secretion of pancreatic or pituitary hormones, it may be preferable to other centrally acting agents and thiazide diuretics for hypertensive patients who are elderly, overweight, or diabetic.
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PMID:Endocrinologic effects of antihypertensive therapy with guanabenz or hydrochlorothiazide. 608 24

In investigating the metabolic adaptation to prolonged exercise in markedly obese subjects, we compared blood glucose, plasma lactate, free fatty acids, insulin and glucagon concentrations during 3 h of treadmill exercise in nine severely obese male patients (OB) (weight excess 84 +/- 7 per cent of their ideal body weight) and in nine healthy controls (C). Speed and slope of treadmill were selected to give a similar oxygen consumption in both groups (OB: 1.61 +/- 0.08 1/min; C: 1.72 +/- 0.07 1/min). Under these conditions, heart rate was similar in both groups, whereas ventilation was significantly lower in overweight subjects. In obese patients, plasma free fatty acid (FFA) levels were higher in the basal state (OB: 740 +/- 43 mumol/l; C: 602 +/- 40 mumol/l, 2 P less than 0.05) but showed a lower increase during the exercise period (OB: + 576 +/- 135 mumol/l; C: + 1071 +/- 100 mumol/l, 2 P less than 0.02). This impaired FFA mobilization was related to significantly higher insulin (IRI) levels throughout the exercise period as shown by the regression line of exercise-induced FFA increase (y, mumol/l) vs mean plasma IRI during exercise (x, microU/ml): y = 1238 - 60 x, r = -0.709, 2 P less than 0.001. Lack of glucagon increase could also contribute to the lower rise of FFA in obese subjects. A correspondingly increased contribution of carbohydrates to the energy supply is suggested by a significant decline in blood glucose and higher lactate plasma concentrations during the second half of the exercise period in overweight patients. These abnormalities could represent a metabolic limitation for performing prolonged exercise in markedly obese patients.
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PMID:Metabolic adaptation to prolonged exercise in severely obese subjects. 688 30


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