Utilizing the GLP-1 signaling system to treat diabetes: Sorting through the pharmacologic approaches

D’Alessio, David A.; Vahl, Torsten

doi:10.1007/s11892-005-0092-2

Cited by 6 publications

(6 citation statements)

References 61 publications

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“…While at a first pass this suggests decreased importance of this peptide as a mechanism for obesity, it becomes important for treatment. Due to their potent effects on improving glucose homeostasis, long-acting GLP-1 agonists are very effective treatments for T2DM and are the only diabetes therapy to decrease body weight [98]. While GLP-1 agonism is efficacious for treatment of T2DM, the contribution of the GLP-1 system to obesity is less clear.…”

Section: Gut-brain Axismentioning

confidence: 99%

Hypothalamic control of energy and glucose metabolism

Sisley

Sandoval

2011

Rev Endocr Metab Disord

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The central nervous system (CNS), generally accepted to regulate energy homeostasis, has been implicated in the metabolic perturbations that either cause or are associated with obesity. Normally, the CNS receives hormonal, metabolic, and neuronal input to assure adequate energy levels and maintain stable energy homeostasis. Recent evidence also supports that the CNS uses these same inputs to regulate glucose homeostasis and this aspect of CNS regulation also becomes impaired in the face of dietary-induced obesity. This review focuses on the literature surrounding hypothalamic regulation of energy and glucose homeostasis and discusses how dysregulation of this system may contribute to obesity and T2DM.

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Section: Gut-brain Axismentioning

confidence: 99%

Hypothalamic control of energy and glucose metabolism

Sisley

Sandoval

2011

Rev Endocr Metab Disord

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“…Секреция инсулина в ответ на пероральный прием глюкозы является более выраженной, чем в ответ на внутривенное введение эквивалентного количества глюкозы [5]. Этот феномен показывает, что желудочно-кишечный тракт (ЖКТ) определенным образом передает информацию о приеме пищи поджелудочной железе, что способствует секреции инсулина в ответ на повыше-ние уровня глюкозы в плазме.…”

Section: инкретиновый эффектunclassified

“…При сахарном диабете недостаточная се-креция инсулина в ответ на повышение уровня глюкозы в плазме крови приводит к недостаточному подавлению секреции глюкагона [11]. ГПП-1 подавляет секрецию глюкагона натощак и после приема пищи, что приводит к снижению концентраций глюкозы в крови натощак [5]. В отличие от ГПП-1, ГИП не ингибирует (а в некоторых случаях может усиливать) секрецию глюкагона [7].…”

Section: эффекты гпп-1unclassified

“…ГПП-1 замедляет скорость опорожнения желудка, что способствует уменьшению колебаний постпран-диальной гликемии [5,9,12]. Угнетение моторики же-лудочно-кишечного тракта и замедление скорости опорожнения желудка, вероятно, опосредовано блуж-дающим нервом [12].…”

Section: эффекты гпп-1unclassified

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Evolution of glucagon-like peptide-1 receptor agonists for the treatment of type 2 diabetes

Galstyan¹,

Karataeva²,

Yudovich³

2017

Diabetes mellitus

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“…In addition, GLP-1 contributes to satiation (22)(23)(24) and regulates gastric function (25,26). GLP-1 is essential for normal glucose tolerance and compounds based on GLP-1 receptor activation have been developed as therapeutics for diabetes (27,28). We therefore reasoned that GLP-1 might be secreted before anticipated meals to augment pre-and postprandial nutrient homeostasis.…”

mentioning

confidence: 99%

Meal-Anticipatory Glucagon-Like Peptide-1 Secretion in Rats

et al. 2010

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Animals anticipating a meal initiate a series of responses enabling them to better cope with the meal's metabolic impact. These responses, such as cephalic insulin, occur prior to the onset of ingestion and are especially evident in animals maintained on a meal-feeding schedule with limited but predictable access to food each day. We tested the hypothesis that meal-fed rats secrete the incretin hormone glucagon-like peptide-1 (GLP-1) cephalically when anticipating a large meal. Male Long-Evans rats were fed ad libitum (controls) or adapted to a schedule on which food was available for the same 4-h period each day (meal fed animals). Plasma GLP-1 increased in meal-fed rats over an interval from 75 to 60 min prior to feeding time, from a baseline of 10 to around 40 pm, and then returned to baseline prior to food presentation. Controls had steady plasma GLP-1 levels (10-15 pm) over the same span. Meal-fed rats also secreted cephalic insulin starting around 15 min prior to food presentation. Administration of the selective GLP-1 receptor antagonist exendin-4[desHis-1,Glu-9] prior to the premeal spike of GLP-1 caused meal-fed rats to eat significantly less food than normal, whereas administration of the antagonist after the GLP-1 spike but prior to food presentation resulted in a significant increase in food consumption. These findings document for the first time a cephalic increase of plasma GLP-1 and suggest that it functions to facilitate consumption of a large meal.

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Utilizing the GLP-1 signaling system to treat diabetes: Sorting through the pharmacologic approaches

Cited by 6 publications

References 61 publications

Hypothalamic control of energy and glucose metabolism

Hypothalamic control of energy and glucose metabolism

Evolution of glucagon-like peptide-1 receptor agonists for the treatment of type 2 diabetes

Meal-Anticipatory Glucagon-Like Peptide-1 Secretion in Rats

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