Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

AO-128 is a potent and structurally novel inhibitor of the intestinal disaccharidases, such as maltase and sucrase. Genetically obese-diabetic mice, KKA(y), were used to examine the acute or long-term effectiveness of this compound. AO-128 decreased a postprandial rise in blood glucose after sucrose solution loading dose-dependently; the ED50 to reduce a delta increment of blood glucose by 50% was 0.22 mg/kg. The intestinal sucrase and maltase activities were suppressed to 7 and 48% of the control levels, respectively, at a dose of 0.21 mg/kg. Four-week-old female KKA(y) mice were kept on a laboratory diet containing 10 or 50 ppm of AO-128 for 12 weeks. The high dose of AO-128 reduced food intake and body weight gain throughout the experimental period. On the other hand, the low dose reduced body weight gain for the first 4 weeks without any effect on food intake. Development of the hyperglycemia and hyperinsulinemia characteristic of KKA(y) mice was moderately prevented by the low dose, and completely by the high dose. Hypertriglyceridemia tended to be suppressed by the AO-128 treatment. The high dose decreased the hemoglobin A1 level and parametrial adipose tissue weight. Hepatomegaly and fatty liver were ameliorated by AO-128 dose-dependently. Nephropathy was ameliorated by the high dose. These findings indicate that AO-128 may be useful for treating human obesity and diabetes.
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PMID:Antiobesity and antidiabetic actions of a new potent disaccharidase inhibitor in genetically obese-diabetic mice, KKA(y). 162 84

The aim of the present study was to evaluate a number of parameters in a group of patients with essential hypertension and then compare the results with those in a group of healthy normotensive subjects. One hundred and fifty-six patients with essential hypertension (EH) in the non-complicated form (73 males, 83) females; mean age: 54.8 +/- 0.9 years) were selected and compared with 150 normotensive subjects matched for age and sex. After a 2-week period of wash-out during which patients followed a diet with normal sodium and calorie content, body mass index, systolic and diastolic arterial pressure (AP), mean arterial pressure (MAP), heart rate in clino- and orthostatism were measured and blood was collected to assay glycemia, total cholesterolemia, LDL and HDL cholesterolemia and triglycerides. In the group of patients suffering from EH all the above parameters were found to be significantly higher than in normotensive control subjects. In particular, in the hypertensive population the prevalence of obesity was 21.3%, hyperglycemia 26.9%, hypercholesterolemia 65.1% and smoking 36.4%. When the possible relation between one or more risk factors and AP values was assessed, it was found that in hypertensive patients the presence of hyperglycemia alone or in association with other metabolic disorders led to the highest MAP findings. Moreover, having studied the correlation rate of the various parameters, it was seen that in both the hypertensive and normotensive populations systolic AP measured in clinostatism positively correlated with glycemia, total cholesterolemia, and age, whereas correlations were not found between clinostatic diastolic AP and the above parameters.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Metabolic changes in the patient with essential hypertension]. 163 Jun 76

A case of advanced cervical carcinoma of the uterus with ectopic adrenocorticotrophic hormone (ACTH) syndrome is described. The patient was seen for general malaise 21 months after surgical treatment of the primary lesion whose histology was undifferentiated small cell carcinoma of the uterine cervix. She had extensive metastases in the liver and the abdominal wall. In addition to the typical clinical manifestations of Cushing's syndrome such as moon face, central obesity and acne vulgaris, hyperglycemia was so severe that she was in a hyperosmolar non-ketotic coma. Endocrinological examinations revealed elevated plasma ACTH and cortisol, and urinary excretion of 17-hydroxycorticosteroids and 17-ketosteroids, which were not suppressed by high-dose dexamethasone administration. Based on these clinical and laboratory findings, a diagnosis of ectopic ACTH syndrome was made. Among the results of other endocrinological examinations conducted to find the etiological cause of the hyperglycemic coma, which seemed to be unusual for ectopic ACTH syndrome, the plasma somatostatin level was abnormally high. Metastatic tumors in the liver obtained at the time of autopsy contained large amounts of both ACTH and somatostatin, and gel filtration studies revealed that the peptides produced by the tumor had the molecular sizes of the biologically active forms of the respective peptides. These observations suggest possible involvement of the somatostatin in deteriorating glucose intolerance to develop hyperglycemic hyperosmolar non-ketotic coma as a drastic disturbance of metabolism.
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PMID:A case of cervical carcinoma of the uterus presenting with hyperosmolar non-ketotic coma as a manifestation of ectopic adrenocorticotropic hormone syndrome. 164 12

Dependent on the dosages used, digestion and absorption inhibitors or disaccharidase inhibitors, such as Acarbose, might cause malabsorption of nutrients, and hence, among other effects, affect caloric balances. This negative effect on caloric balance has actually been well documented in animal experimentation. However, in nondiabetic subjects with excessive degrees of obesity, no consistent weight reduction could be induced by disaccharidase inhibitors. Subsequently, Acarbose has been advocated for type 2 diabetic patients in dosages that might reduce postprandial hyperglycemia and insulinemia, whereas significant degrees of malabsorption should be excluded. At these dosages of the drug, there is no clinical perspective with regard to weight-reducing (side) effects of disaccharidase inhibitors. Whether a hypothetical diminution of serum insulin daily profiles during Acarbose treatment in obese type 2 diabetic patients might contribute to a normalization of the metabolic syndrome and to a facilitation of weight-reducing efforts remains speculative. At present, there does not seem to be much rationale in trying to exploit digestion and/or absorption inhibitors for weight-reduction therapies in obesity, unless they are used to enforce a negative caloric balance by malabsorption of nutrients.
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PMID:Pharmacological treatment of obesity: digestion and absorption inhibitors-clinical perspective. 172 47

The aim of the present study was to evaluate the prevalence of certain cardiovascular risk factors in the population of Asepeyo-Elche. The study sample was a working population of 697 persons (71.8% males and 28.2% females) with ages ranging from 15 to 65 years (mean age 34.7 +/- 13.2 years), seen during the first 6 months of 1990 in the health care center of Asepeyo-Elche. The evaluated cardiovascular risk factors and their prevalence rates were: hypertension (14.2%), hypercholesterolemia (18.5%), smoking (52.5%), hyperglycemia (3.5%), obesity (28.2%) and sedentariness (80.3%). We conclude that in our working population the prevalence rates of some cardiovascular risk factors are high and that intervention programs to modify the diet and lifestyle are mandatory to prevent the pathogenetic consequences of these factors.
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PMID:[Cardiovascular risk factors in the working population of Alicante]. 175 30

Late diabetic effects are the sequelae of for a long time super elevated blood sugar levels. The diabetic nephropathy is the cause of the secondary arterial hypertension. The investigation seeks for the connections between the diabetes mellitus and the essential, that is primary hypertension. The two diseases frequently appear and clearly increase in the second half of life. Moreover, they are above average frequently associated with each other. Among brothers and sisters of diabetic hypertensives in comparison to normal cohorts clearly increased high blood pressure prevalences were found. The insulin resistance which could be proved in a great number of hypertensive and which has been known since more than two decades might be the connecting link between hypertension and diabetes mellitus. Like the obesity the essential hypertension can be associated with all degrees of an insulin hyposensitiveness. The sodium-retaining effect of the insulin might explain the increased sodium content of the body in hypertensives. The differential diagnostics of the essential hypertension should therefore seek for conditions of an insulin resistance. The type II diabetic lacks a release of bradykinin during muscle work. Thus the glucose uptake into the cell is unfavourable influenced and demands an increased insulin excretion. This genetically (?) fixed defect is found also in essential hypertensives. It could be the connecting link between the two diseases. ACE-inhibitors have via a kininase II inhibition an effect also on the bradykinin decomposition and can favourable influence the glucose uptake into the muscle. An improved insulin effect among the ACE-inhibitors was described. Therefore, they should be preferred in the treatment of hypertensive diabetics.
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PMID:[Diabetes mellitus and arterial hypertension. In search of the connecting link]. 177 26

The total energy expenditure (EE) of human beings is represented by basal metabolic rate (which corresponds to 60-70% of EE), dietary-induced thermogenesis (10% of EE), and the energy expended in physical activity (20-30% of EE). Obese individuals have an increased total EE compared with lean subjects; this increase is essentially due to an increased lean body mass concomitant with obesity, and is completely reverted after weight loss. Glucose-induced thermogenesis (GIT), measured during an oral glucose tolerance test (OGTT) or hyperinsulinemic-euglycemic clamps, has been found to be decreased in obese individuals, although some discrepancy exists between studies. The observed decreases in GIT show a gradation, increasing progressively from obese patients with normal glucose tolerance to obese patients with impaired glucose tolerance (IGT) to obese patients with non-insulin-dependent diabetes mellitus (NIDDM) and an increased insulin response after OGTT to obese patients with NIDDM and a hypoinsulinemic response after OGTT. The defect in GIT appears to be related to impairment in nonoxidative glucose storage and with the degree of insulin resistance. Obese patients after weight loss show a further decrease in GIT after OGTT or during a euglycemic clamp, which remains unclear. Obese patients have an increased basal lipid oxidation and a decreased suppression of lipid oxidation after OGTT or during a euglycemic clamp. Glucose oxidation and storage are both markedly decreased during a euglycemic clamp. In contrast, the defect in glucose storage is less apparent after OGTT, due to the compensatory effect of hyperglycemia and hyperinsulinemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Energy and substrate metabolism in obesity and postobese state. 177 3

Four patients with granulomatous disease of the anterior visual pathway presented with optic neuropathy between July 1986 and February 1987, secondary to an orbital pseudotumor (n = 1) and sarcoidosis (n = 3). All but one became resistant to corticosteroid therapy, and all were subsequently treated for 1 to 2 years with low-dose cyclosporine alone or in combination with tapering doses of prednisone. Two patients experienced pronounced recovery of visual function, and visual function was stabilized in the other two; in one of these, magnetic resonance imaging showed substantial regression of intracranial lesions. Steroid-induced complications of uncontrolled hyperglycemia (n = 2) and obesity (n = 4) were controlled with cyclosporine. The authors conclude that low-dose cyclosporine is a safe and effective therapeutic alternative in ocular granulomatous diseases.
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PMID:Low-dose cyclosporine therapy of granulomatous optic neuropathy and orbitopathy. 180 Sep 35

Conflicting information concerning the acute effect of hyperinsulinemia on circulating adrenal androgens, specifically DHEAS, is available. The effect of PCOD or obesity on this response is unclear. We prospectively examined the acute response of circulating DHEAS to the physiological rise in serum insulin after an OGTT in 10 women with PCOD (5 obese and 5 normal weight) and 10 ovulatory euandrogenic women (5 obese and 5 normal-weight). All underwent a standard 75-g 2-hour OGTT. Insulin and DHEAS were measured before and after OGTT. To control for the potential dilutional effects induced by hyperinsulinemia or hyperglycemia on intravascular tonicity, DHEAS levels were correlated to serum protein. As expected, the 2-hour insulin levels were significantly greater than baseline. No significant changes in circulating DHEAS or in the DHEAS to protein ratio was observed in any patient group 2 hours after glucose-induced hyperinsulinemia. The power of this study was greater than 89% for an alpha error of 0.05 and an expected change in DHEAS of 25%. In summary, it appears unlikely that acute increases in insulin within the physiological range are important in the regulation of circulating DHEAS in either PCOD or euandrogenic women, independent of obesity.
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PMID:No acute effect of physiological insulin increase on dehydroepiandrosterone sulfate in women with obesity and/or polycystic ovarian disease. 183 37

This study was performed to examine the effect of overeating on in vivo and in vitro insulin secretion in normal mice. Six week old male CRJ-ICR mice were maintained on a cookie and chocolate mashed diet (C.C. diet) until 30 weeks of age; control mice received an ordinary mouse chow. The mice on the C.C. diet (C.C. mice) consumed 125-130% of the daily caloric intake of control mice throughout the study. C.C. mice developed mild hyperglycemia with relative obesity from 16 weeks of age. Fed blood glucose levels at 30 weeks of age for C.C. mice were 158.3 +/- 6.7 mg/dl as opposed to 127.2 +/- 3.1 mg/dl for controls (p less than 0.01). In experimental mice at 18 weeks of age, plasma insulin response after intraperitoneal glucose load (2 mg/g BW) and insulin secretion at 30 mM glucose from the perfused pancreas were similar to those in control mice. However, at 30 weeks of age, insulin secretion at 30 mM glucose from perfused pancreas in C.C. mice was significantly suppressed compared with that of control mice (p less than 0.02). Conversely, in vivo insulin secretory response to intraperitoneal glucose load was significantly increased in C.C. mice (p less than 0.05). There were no differences in insulin secretion at 15 mM glucose from perfused pancreas. These results indicate that impairment of beta-cell secretory capacity develops in impaired glucose tolerant mice with obesity, while in vivo studies show a high insulin response to glucose. This alteration of beta-cell function may be the initial change during the development of the hyperglycemia-induced defect in insulin secretion.
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PMID:The effects of overeating on insulin secretion in normal mice. 184 Oct 30


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