Bromocriptine (Ergoset) Reduces Body Weight and Improves Glucose Tolerance in Obese Subjects

Cincotta, Anthony H.; Meier, Albert

doi:10.2337/diacare.19.6.667

Cited by 119 publications

(113 citation statements)

References 16 publications

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“…Two weeks of bromocriptine treatment reduced body weight (from 223.4g to 210.4g, P < 0.02), while the weight of the vehicle treated animals remained the same (from 222.6g to 221.9g, P = 0.9), to produce a between group difference in change from baseline body weight of -12.3g (P < 0.001) without altering food consumption (11.0g vs. 10.3g per day, P = 0.3) as has been repeatedly reported in these animals [1][2][3].…”

Section: Resultssupporting

confidence: 51%

“…Timed daily systemic or intracerebroventricular administration of bromocriptine, a dopamine D2 receptor agonist, to hyperinsulinemic, insulin resistant animals or once daily (morning) systemic administration of bromocriptine-QR, a quick release formulation of bromocriptine to such humans improves fasting hyperinsulinemia and impaired glucose tolerance by simultaneously reducing post glucose challenge plasma glucose and insulin levels [1][2][3][4]. However in these studies, fasting plasma glucose reductions in response to such treatment varied from not at all to moderate depending upon the prevailing glucose level.…”

Section: Introductionmentioning

confidence: 99%

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Weighted Effects of Bromocriptine Treatment on Glucose Homeostasis during Hyperglycemic versus Euglycemic Clamp Conditions in Insulin Resistant Hamsters: Bromocriptine as a Unique Postprandial Insulin Sensitizer

Ezrokhi¹,

Luo²,

Trubitsyna³

et al. 2012

J Diabetes Metab

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Background: Postprandial glucose metabolism is deranged in insulin resistant states typified by increased hepatic glucose output and reduced peripheral and hepatic glucose deposition despite elevated plasma insulin levels. And, mounting evidence suggests that postprandial hyperglycemia may potentiate cardiovascular disease. Time-of-day pulsed bromocriptine (a dopamine D2 receptor agonist) administration to insulin resistant animals and humans improves impaired glucose tolerance and post-meal hyperglycemia without raising the plasma insulin level when assayed many hours after bromocriptine has been removed from the circulation. The bromocriptine response of glucose lowering is more prominent after a meal than just before the meal suggesting a "weighted" effect on postprandial glucose metabolism. However, this supposition has never been evaluated under controlled physiological glucose-insulin clamp conditions to verify the existence of such a unique phenomenon. Findings:This study therefore investigated the effects of daily bromocriptine or vehicle administration for 2 weeks on hepatic glucose output and total body glucose disposal during such hyperglycemic versus euglycemic insulin clamp conditions in insulin resistant, glucose intolerant Syrian hamsters. Bromocriptine treatment improved fasting insulin sensitivity (HOMA-IR) by 38% P < 0.04 and both total body glucose disposal and hepatic glucose output during the euglycemic clamp by 21% and 26%, P < 0.03 respectively, relative to vehicle treated animals. Importantly, the incremental increase in total body glucose disposal and inhibition in hepatic glucose output under hyperglycemic versus euglycemic conditions was greater (73% vs. 40%, P < 0.001) and markedly stronger (30% vs. no change, P < 0.002), respectively, in bromocriptine versus vehicle treated animals, respectively. Conclusions:These findings indicate a unique hyperglycemic environment "weighted" effect of bromocriptine on improving glucose homeostasis in insulin resistant animals that is independent of plasma insulin level.

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Section: Resultssupporting

confidence: 51%

Section: Introductionmentioning

confidence: 99%

Weighted Effects of Bromocriptine Treatment on Glucose Homeostasis during Hyperglycemic versus Euglycemic Clamp Conditions in Insulin Resistant Hamsters: Bromocriptine as a Unique Postprandial Insulin Sensitizer

Ezrokhi¹,

Luo²,

Trubitsyna³

et al. 2012

J Diabetes Metab

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“…The mechanisms by which lower prolactin levels could contribute to the development of obesity are not clear. Paradoxically, bromocryptine reduces both prolactin and body weight in obese patients (48). As bromocryptine also modulates seratonin and norepinephrine within the hypothalamus (49), the effects on obesity may be mediated through central rather than peripheral mechanisms.…”

Section: Analysis Of Genes Regulated By Both Obesity and Leptinmentioning

confidence: 99%

Quantitative Expression Analysis of Genes Regulated by Both Obesity and Leptin Reveals a Regulatory Loop between Leptin and Pituitary-derived ACTH

Renz¹,

Tomlinson²,

Hultgren³

et al. 2000

Journal of Biological Chemistry

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Absence of the hormone leptin leads to dramatic increases in appetite, food intake, and adiposity. The primary site of action, at least with respect to appetite, is the hypothalamus. Leptin also has significant effects on the function(s) of peripheral organs involved in maintaining body composition. Some of these effects are mediated through direct interaction of leptin with its receptor on the target tissue, and some effects are indirectly mediated through secondary hormonal and neural pathways. Few of the genes that are responsible for regulating body composition and the peripheral effects of leptin are known. We have used a new gene profiling technology to characterize gene expression changes that occur in the pituitary, hypothalamus, fat, muscle, and liver in response to both obesity and treatment with exogenous leptin. These differences were then overlaid to allow the identification of genes that are regulated by obesity and at least partially normalized by leptin treatment. By using this process we have identified five genes (POMC, PC2, prolactin, HSGP25L2G, and one novel) that are both abnormally expressed in the pituitaries of obese mice and are sensitive to the effects of leptin. We also show that adrenocorticotropic hormone appears to be involved in a regulatory loop involving leptin.

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“…Há estudos em animais, nos quais a secreção de prolactina está associada a acúmulo de gordura em pássaros na fase pré-migratória e em mamífe-ros na fase de pré-hibernação. Baseado nesses dados, foi conduzido um estudo com a bromocriptina que documentou perda de peso e redução de pregas cutâneas em relação a placebo (73).…”

Section: A Norepinefrinaunclassified

Aspectos fisiológicos do balanço energético

Mancini

Halpern

2002

Arq Bras Endocrinol Metab

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RESUMOconhecidos. Nesta revisão, abordamos os nutrientes, monoaminas e peptídeos que podem levar a redução da ingestão e, em alguns casos, aumentar a ingestão de alimentos. Vários desses mecanismos podem levar ao desenvolvimento de novas abordagens no tratamento da obesidade ou na elucidação do mecanismo de ação de agentes farmacológicos. NUTRIENTES Agentes de Ação Periférica a. Análogos e metabólitos da hexoseA teoria glicostática (1) propõe que taxas de utilização de glicose podem ser sinais para iniciar ou ultimar a ingestão alimentar.Glicose. Uma diminuição no nível de glicose pode preceder e iniciar a alimentação em animais e humanos (2,3). Infusões periféricas de glicose diminuem a ingestão alimentar em animais experimentais, sendo o nervo vago a conexão entre os glicorreceptores periféricos e o cérebro. Quando glicose é infundida na circulação portal, a descarga de aferentes vagais é reduzida à medida que a concentração de glicose aumenta (4). A infusão de glicose ou arginina diminui a taxa de transmissão aferente e aumenta a transmissão simpática eferente ao tecido adiposo marrom (5).

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Bromocriptine (Ergoset) Reduces Body Weight and Improves Glucose Tolerance in Obese Subjects

Abstract: When combined with instruction to follow a moderate hypocaloric diet, Ergoset, but not placebo, improves glucose tolerance and promotes significant weight and body fat loss in obese subjects over an 18- week treatment period.

Cited by 119 publications

References 16 publications

Weighted Effects of Bromocriptine Treatment on Glucose Homeostasis during Hyperglycemic versus Euglycemic Clamp Conditions in Insulin Resistant Hamsters: Bromocriptine as a Unique Postprandial Insulin Sensitizer

Weighted Effects of Bromocriptine Treatment on Glucose Homeostasis during Hyperglycemic versus Euglycemic Clamp Conditions in Insulin Resistant Hamsters: Bromocriptine as a Unique Postprandial Insulin Sensitizer

Quantitative Expression Analysis of Genes Regulated by Both Obesity and Leptin Reveals a Regulatory Loop between Leptin and Pituitary-derived ACTH

Aspectos fisiológicos do balanço energético

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