Plasma Ghrelin Concentrations Are Not Regulated by Glucose or Insulin

Schaller, Georg; Schmidt, Alice; Pleiner, Johannes; Woloszczuk, W.; Wolzt, Michael; Luger, Anton

doi:10.2337/diabetes.52.1.16

Cited by 185 publications

(142 citation statements)

References 49 publications

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“…Our data regarding ghrelin levels during the OGTT are in accordance with previous data showing that insulin is a key regulator of the postprandial ghrelin suppression response [8], although some controversy surrounds this topic [9]. To date, studies (at least in humans) indicate that supraphysiological or prolonged peripheral insulin administration affects the plasma ghrelin concentration [10]. However, physiological short-term peripheral insulin elevation had no effect on ghrelin levels in most of these studies [9,10].…”

Section: Discussionsupporting

confidence: 90%

“…To date, studies (at least in humans) indicate that supraphysiological or prolonged peripheral insulin administration affects the plasma ghrelin concentration [10]. However, physiological short-term peripheral insulin elevation had no effect on ghrelin levels in most of these studies [9,10]. Our data show that during the OGTT the elevations in the plasma insulin level are able to induce insulin signalling in the hypothalamus, as demonstrated by increased IR tyrosine phosphorylation and Akt serine phosphorylation in this tissue.…”

Section: Discussionmentioning

confidence: 54%

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Circulating ghrelin concentrations are lowered by intracerebroventricular insulin

et al. 2006

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Aims/hypothesis Ghrelin is a peptide that is mainly produced by the stomach and stimulates food intake, adiposity and weight gain. Previous studies have documented that plasma levels of ghrelin are reduced by insulin, but the mechanisms that mediate this effect are unclear. Methods To determine whether phosphatidylinositol 3-kinase (PI(3)K) and/or mitogen-activated protein kinase (MAPK) are involved in this insulin action, we tested the intracerebroventricular (i.c.v.) effect of specific inhibitors of PI(3)K (LY294002 and wortmannin) and MAPK (PD98059 and UO126) on the insulin-mediated reduction of ghrelin levels in rats. Results Intracerebroventricular treatment with insulin reduced ghrelin levels. Inhibition of PI(3)K specifically blocked the insulin-induced reduction in ghrelin concentration, whereas inhibition of MAPK had no effect on insulinmediated actions. Moreover, pretreatment with i.c.v. PI(3)K inhibitors blocked the reduction of ghrelin levels after OGTT-induced hyperglycaemia and hyperinsulinaemia. Conclusions/interpretation These data demonstrate that changes in insulin action in the central nervous system regulate circulating ghrelin levels and that PI(3)K is a specific mediator of this action.

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Section: Discussionsupporting

confidence: 90%

Section: Discussionmentioning

confidence: 54%

Circulating ghrelin concentrations are lowered by intracerebroventricular insulin

et al. 2006

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“…A decrease of insulin in a reduced obesity state may lead to an increase in hunger and desire to eat (Tremblay and Doucet, 2000;Benoit et al, 2004;Strader and Woods, 2005). Our results do not indicate that postprandial decline in ghrelin levels is mediated by insulin, which is in accordance with some (Purnell et al, 2003;Schaller et al, 2003), but not all (Saad et al, 2002) previously performed studies. Ghrelin responses are modified by fat intake.…”

Section: Discussionsupporting

confidence: 50%

Arabinoxylan consumption decreases postprandial serum glucose, serum insulin and plasma total ghrelin response in subjects with impaired glucose tolerance

Otto²,

et al. 2006

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Objective: Arabinoxylan (AX) consumption is associated with metabolic improvement during diabetes and with modulation of ghrelin, an orexigenic gut hormone. The effect of AX consumption on ghrelin secretion in disturbed metabolic states is unknown. Therefore, we investigated the postprandial responses to AX consumption of serum glucose, insulin and triglycerides and plasma total and acylated ghrelin in subjects with impaired glucose tolerance (IGT). Design: Randomized, single-blind, controlled, crossover intervention trial. Subjects: Seven female and four male adults with IGT, aged 55.5 years, and body mass index (BMI) 30.1 kg/m 2 . Intervention: Subjects received either placebo or 15 g AX supplement for 6 weeks with a 6-week washout period in-between. Main outcome measurements: Postprandial responses of serum glucose, insulin and triglycerides, and plasma total and acylated ghrelin after a liquid meal challenge test (LMCT) measured at the beginning and at the end of the dietary intervention at À20, À5, 0, 15, 30, 45, 60, 90, 120, 150, 180, 210 and 240 min. Results: After LMCT, AX consumption resulted in lower postprandial responses in serum glucose, insulin and triglycerides (Po0.05). Compared to placebo, total plasma ghrelin was also reduced by 4278 pg/ml (Po0.001) after AX consumption with no difference in plasma acylated ghrelin. Conclusion: AX consumption improved postprandial metabolic responses after an LMCT in subjects with IGT and reduced total ghrelin response. However, acylated ghrelin responses were unchanged, suggesting that the acylated ghrelin-mediated orexigenic regulation is not improved as only total plasma ghrelin decreased. Sponsorship: Federal Ministry of Education and Research Germany (PTJ-BIO/0313042C).

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“…Details of the experimental procedure have been published previously [10]. On three different study days subjects received infusions of insulin, somatostatin or placebo with a washout phase of at least 2 days.…”

Section: Experimental Protocolmentioning

confidence: 99%

The release of the adipocytokine visfatin is regulated by glucose and insulin

et al. 2006

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Aims/hypothesis The novel insulin-mimetic adipocytokine visfatin has been linked to the metabolic syndrome, but its regulation has not been characterised to date. Since insulinmimetic actions of visfatin may be part of the feedback regulation of glucose homeostasis, we hypothesised that visfatin concentrations are influenced by glucose or insulin blood levels in humans. Subjects, materials and methods In this randomised, doubleblind, placebo-controlled crossover study, nine healthy male subjects (age 26±6 years) attended three different study days. On each day, systemic glucose concentrations of 5.0, 8.3 and 11.1 mmol/l were attained by stepwise increases in i.v. infusions of glucose, representing fasting and postprandial conditions. Visfatin plasma concentrations were studied during concomitant exogenous hyperinsulinaemia, inhibition of endogenous insulin production by somatostatin infusion, and placebo time control. Additionally, human adipocytes were cultured to study visfatin release and mRNA expression in vitro.Results Glucose concentrations of 8.3 and 11.1 mmol/l increased circulating visfatin from baseline concentrations of 0.5±0.0 ng/ml to 0.9±0.1 and 2.1±0.3 ng/ml, respectively (p<0.01). Glucose-induced elevation of visfatin was prevented by co-infusion of insulin or somatostatin (p<0.05). Cultured subcutaneous and visceral adipocytes released an equivalent amount of visfatin upon glucose-concentrationand time-dependent stimulation. Visfatin secretion involved the phosphatidylinositol 3-kinase (PI3-kinase) and protein kinase B (AKT) pathways. The mRNA expression pattern of visfatin was consistent with this altered protein release. Conclusions/interpretation Circulating visfatin concentrations are increased by hyperglycaemia. This effect is suppressed by exogenous hyperinsulinaemia or somatostatin infusion. Glucose signalling for visfatin release in adipocytes involves the PI3-kinase/AKT pathway.

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Plasma Ghrelin Concentrations Are Not Regulated by Glucose or Insulin

Cited by 185 publications

References 49 publications

Circulating ghrelin concentrations are lowered by intracerebroventricular insulin

Circulating ghrelin concentrations are lowered by intracerebroventricular insulin

Arabinoxylan consumption decreases postprandial serum glucose, serum insulin and plasma total ghrelin response in subjects with impaired glucose tolerance

The release of the adipocytokine visfatin is regulated by glucose and insulin

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