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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors report a girl with acute lymphoblastic leukaemia presenting hypothalamic syndrome characterized by meningeal leukaemia, hyperphagia and obesity. Insulin and growth hormone secretion, studied with arginine and insulin stimulation tests, showed a high peak of serum insulin and no response of growth hormone. Insulin and growth hormone responses to these tests reverted to normal after intrathecal methotrexate.
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PMID:Insulin and growth hormone secretion in a leukaemic girl with hypothalamic syndrome. 26 33

Obesity in the Zucker rat is accompanied by hyperlipemia, hyperinsulinism, insulin resistance, pancreatic hyperplasia, and islet hypertrophy. This study correlates the morphologic heterogeneity of isolated pancreatic islets with secretion of insulin and glucagon in the perifusion system. Islet size was arbitrarily defined as large (greater than 0.45 mm) or small (smaller than 0.12 mm). Protein content and volume (V = 4/3pir3) were calculated for groups and individual islets, respectively. Islets from obese rats secreted more insulin in response to glucose and aminophylline than islets from lean rats (peak 7.8 +/- 2.4 vs. 1.5 +/- 0.37 microU/islet/min, P less than 0.005). Insulin release was related directly to islet size and protein content. Small islets from lean and obese animals produced less insulin per islet than large islets (P less than 0.005). In terms of islet volume, however, large islets were inefficient insulin releasers as compared to small islets (P less than 0.005). Stimulation with Br-cAMP released glucagon from islets of lean but not from large islets of obese animals (peak 11 +/- 3.3 vs. 4.1 +/- 0.3 pg/microgram protein per minute, P less than 0.05). Arginine produced the same effect on glucagon release (P less than 0.05) as stimulation with Br-cAMP. The observed increased insulin release rates and the blunted glucagon response are related to islet size in the pancreas of the Zucker rat.
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PMID:Correlation between morphology and function in isolated islets of the Zucker rat. 37 79

Plasma glucose, immunoreactive insulin (IRI), and growth hormone (GH) were determined in fasted lean and genetically obese pigs at 1, 3, and 6 mo of age. Rate of glucose clearance and plasma IRI and GH response in provocative stimulation were also measured. Fasting glucose was similar in lean and obese pigs, whereas glucose clearance rate was more rapid in lean pigs. Obese pigs were not hyperinsulinemic but had lower plasma GH than lean pigs. At 1 mo of age, both lean and obese pigs had higher plasma IRI and GH as compared to 3 and 6 mo. Glucose infusion produced increases in plasma IRI at 1, 3, and 6 mo, respectively, with the greatest increases at 6 mo. Plasma IRI peaked at the same level in both pig types at a given age; but due to a more prolonged response in obese pigs, the overall IRI response to glucose infusion was greater in obese pigs. Arginine infusion caused much smaller IRI responses than glucose, but the response of obese pigs was significantly greater than that of lean pigs. Both provocative stimuli caused increases in plasma GH. The GH response to glucose infusion in obese pigs was considerably less than in lean pigs. These observations suggest mild insulin insensitivity and a reduced GH secretory potential in the obese as compared to lean pigs.
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PMID:Insulin and growth hormone in lean and obese pigs. 88 46

The pattern of insulin response to oral and/or intravenous glucose has been claimed to be characteristic of diabetes and even prediabetes. To determine if differences in insluin secretion might explain the exceptionally high prevalence of diabetes in the Pima Indians, 26 genetically normal Pimas (nondiabetic offspring of nondiabetic parents), 32 genetically prediabetic Pimas (nondiabetic offspring of diabetic parents), 10 diabetic Pimas, and 29 normal Caucasians were studied. All subjects received an intravenous glucose tolerance test (IVGTT) to examine the acute-phase insulin response, and all nondiabetic subjects received an oral glucose tolerance test (OGTT) and arginine infusion (AI). The prediabetics also received a cortisone-primed oral glucose tolerance test (CGTT) and were classified by the result of this test. While acute-phase insulin release during the IVGTT was absent in the diabetics, there was a rapid response in all nondiabetics. Prediabetic Pimas with normal or abnormal CGTT had insulin levels similar to normal Indians during the IVGTT, OGTT, and AI. Thus, no evidence of impairment of acute- or late-phase insulin release was found. The normal and prediabetic Indians had fasting and stimulated insulin levels during all the tests two-to-threefold greater than the Caucasians. Differences in insulin levels between the two races could not be explained by differences in glucose level, age, or obesity.
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PMID:Unexplained hyperinsulinemia in normal and "prediabetic" Pima Indians compared with normal Caucasians. An example of racial differences in insulin secretion. 89 36

Long term feeding of a sucrose rich diet to rats is accompanied by a decreased glucose assimilation rate, despite high plasma insulin levels. Hyperinsulinism is at least partially based on a relative obesity, with increased amounts of abdominal- and retroperitoneal fat tissue, but unchanged total body weight compared to starch fed controls. The secretory pattern of insulin release was studied following glucose, arginine, fructose and sulfonylurea administration in the isolated perfused pancreas of sucrose and isocaloric starch fed rats. In addition, isolated islets of Langerhans were used to demonstrate the effects of glucose on insulin secretion and the incorporation of H-3 leucine into the proinsulin and insulin fraction of islet proteins. Following 11 mM glucose, the dynamics of insulin release in the isolated perfused pancreas of sucrose fed rats is characterized by a markedly elevated, late plateau-like response, usually seen only at higher glucose concentrations. Hyperinsulinism, as compared to starch fed controls, can also be demonstrated following arginine and the sulfonylurea HB-419, whereas fructose has no effect in the presence of low glucose concentrations. During incubation of the pancreatic islets, the hyperinsulinism in sucrose-, compared to starch fed rats, is more pronounced at 11 mM glucose than at 5.5 mM glucose. The incorporation of H-3 leucine into the proinsulin-insulin fraction of islet proteins in sucrose compared to starch fed rats, however, is significantly greater with glucose 5.5 mM than at high glucose level. In sucrose fed rats, secretion and biosynthesis of insulin thus appear to be elevated but closely linked only at physiological glucose concentration.
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PMID:Insulin secretion and biosynthesis in sucrose fed rats. 97 34

1. Fatty acid synthesis, measured in the perfused liver of genetically obese (ob/ob) mice with 3H2O or [14C]actate, did not show the inhibition by [8-arginine]vasopressin (antidiuretic hormone) that is observed in livers from normal mice. 2. Hepatic glycogen breakdown in obese mice was stimuulated by vasopressin, but not as extensively as in lean mice. 3. If obese mice received a restricted amount of food, then fatty acid synthesis still did not respond to vasopressin, but glycogen breakdown was fully stimulated. 4. Cholesterol synthesis was not inhibited by vasopressin in livers from obese mice. 5. Vasopressin inhibited fatty acid synthesis in intact lean mice, but not in obese animals. 6. These results suggest that genetic obesity could be due to an inborn error within the mechanisms (other than adenylate cyclase) which mediate responses to extracellular effectors.
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PMID:Resistance to hepatic action of vasopressin in genetically obese (ob/ob) mice. 100 43

These studies demonstrate that the competitive antagonist of nitric oxide synthesis, L-NG-nitro-arginine methyl ester (NO Arg ME), produces an L-arginine reversible decrease in food intake in mice. NO Arg ME also blocked the feeding effect of the potent orexigenic peptide, neuropeptide Y. NO Arg ME produced weight loss when administered over 5 days. The studies suggest that nitric oxide is a physiological modulator of food intake and that nitric oxide synthetase inhibitors may be useful in the management of obesity.
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PMID:Competitive antagonism of nitric oxide synthetase causes weight loss in mice. 138 64

A blunted growth hormone (GH) response to several stimuli, including growth hormone-releasing hormone (GHRH), has been shown in obesity. Arginine (ARG) has been demonstrated to potentiate the GHRH-induced GH increase in normal subjects, likely acting via inhibition of hypothalamic somatostatin release. To shed further light onto the mechanisms underlying the blunted GH secretion in obesity, we studied the effect of ARG (0.5 g/kg infused intravenously [IV] over 30 minutes) on both basal and GHRH (1 micron/kg IV)-stimulated GH secretion. Eight obese subjects (aged 26.4 +/- 3.9 years; body mass index, 39.0 +/- 1.9 kg/m2) and eight normal control volunteers (aged 27.0 +/- 1.7 years; body mass index, 22.3 +/- 0.5 kg/m2) were studied. In obese subjects, the GH response to both GHRH and ARG was lower (P less than .01 and P less than .002, respectively) than in controls. ARG potentiated the GH response to GHRH in obese patients (P less than .0003). However, in these patients, the GH secretion elicited by GHRH, even when coadministered with ARG, persisted at reduced levels (P less than .005) when compared with controls. Basal insulin-like growth factor-1 (IGF-1) levels did not significantly differ in obese subjects and in normal subjects (161.1 +/- 37.0 v 181.0 +/- 12.8 micrograms/L). In conclusion, ARG enhances the blunted GHRH-induced GH increase in obese patients, but the GH responses to ARG alone and to ARG + GHRH persist at lower levels than in normals. Thus, our results suggest the existence of a reduced pituitary GH pool in obesity.
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PMID:Arginine potentiates but does not restore the blunted growth hormone response to growth hormone-releasing hormone in obesity. 158 39

Health providers examining children of short stature should assess adequacy of growth, determine growth rate, and predict final height with treatment. They can use established standards of growth to compare the child's height with that of other children of the same age to assess growth normalcy. If the child's height is lower than the 3rd/5th percentiles, the health provider must also determine whether the growth velocity is 3 cm/year by following the child for 6 months to 1 year, and whether retardation of skeletal maturity is of more than 2 bone age years to confirm abnormal growth. while the child is being followed for growth velocity, the health provider should prescribe a balanced nutritious diet. If these conditions are met and the child exhibits facial characteristics of growth hormone (GH) deficiency, central obesity, unusually small lower jaw, and prepuberal sex characteristics and behavior after usual age of puberty, the health provider can diagnose GH deficiency. 17% of children of short stature in a certain area of India have GH deficiency. The actual height, chronological age, and bone age are needed to predict the final adult height to monitor the impact of GH therapy. GH levels of less than 7 ng/ml in children not suffering from protein malnutrition suggest total GH deficiency. GH measurements must be done over 24 hours, since GH secretion is pulsatile. Sleep, exercise, and intravenous infusion of 0.5 g/kg body weight of arginine stimulates GH secretion. The most common pharmacologic tests to determine GH secretory status include insulin hypoglycemia and clonidine. Clonidine induces fewer side effects and is more safe than insulin hypoglycemia. Since a child can secrete normal amounts of GH with insulin hypoglycemia, the health provider should conduct 1 physiologic (sleep/exercise) test and 1-2 pharmacologic tests to diagnose GH deficiency.
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PMID:Diagnosis of GH deficiency: auxologic and GH response criteria. 182 77

Nitric oxide (NO) may be an intercellular modulator within the central nervous system. L-arginine, which results in NO synthesis, increased food intake in mice while the inhibitor of NO synthesis, L-NG-nitro arginine (L-NO Arg) inhibited food intake in food deprived mice. L-arginine, but not D-arginine, partially reversed the inhibitory effect of L-NO Arg on food intake. These findings suggest the possibility that NO may be a physiological modulator of food intake and that the possibility of exploring the utility of L-NO arg in the treatment of obesity should be explored.
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PMID:Evidence that nitric oxide modulates food intake in mice. 187 80


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