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David H St-Pierre, Rémi Rabasa-Lhoret, Marie-Ève Lavoie, Antony D Karelis, Irene Strychar, Eric Doucet and Lise Coderre


Ghrelin levels are decreased upon food intake, but the impact of specific diet-derived macronutrients on its regulation remains unclear. In addition, because of ghrelin's association with body weight regulation, it is important to understand the mechanisms regulating its levels in obese individuals.


To examine the effect of specific macronutrients on ghrelin levels in overweight and obese postmenopausal women.


Thirty-five subjects underwent a euglycemic/hyperinsulinemic clamp (EHC) to examine glucose disposal and total ghrelin (TotG) and acylated ghrelin (AG) levels. Macronutrient intake was evaluated with a 3-day food questionnaire.


Under fasting conditions, positive associations were observed between fiber intake and TotG and AG levels. Fasting AG also correlated positively with the intake of total energy, as well as monounsaturated and polyunsaturated lipids. Importantly, fiber consumption explained up to 26 and 23% of the variation in TotG and AG respectively. During the EHC, TotG levels were significantly reduced at all times, while AG was decreased at 60 min only. TotG area under the curve (AUC) values were positively associated with fiber and polyunsaturated lipid intake, while AG AUC values correlated positively with fiber, total energy, carbohydrate, and lipid intake. Interestingly, fiber intake explained up to 21% of the variation in TotG AUC, while total energy intake predicted up to 21% of the variation in the AG AUC.


The present study suggests that fiber intake is an important regulator of ghrelin levels both in fasting and in hyperinsulinemic conditions. Overall, these results reinforce the importance of the intimate association between eating habits and gastrointestinal hormonal regulation.

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David H St-Pierre, Jean-Philippe Bastard, Lise Coderre, Martin Brochu, Antony D Karelis, Marie-Éve Lavoie, Florin Malita, Jonathan Fontaine, Diane Mignault, Katherine Cianflone, Pascal Imbeault, Éric Doucet and Rémi Rabasa-Lhoret

Objective: Recent reports have suggested that the existence of associations between hormonal dysregulation and chronic upregulation of inflammatory markers, which may cause obesity-related disturbances. Thus, we examined whether acylated ghrelin (AcylG) and total ghrelin (TotG) levels could be associated with the following inflammatory markers: C-reactive protein (CRP), tumor necrosis factor α (TNF-α), and soluble TNF receptor 1 (sTNF-R1).

Design: Cross-sectional study consisting of 50 overweight and obese postmenopausal women.

Methods: AcylG and TotG levels were assessed at 0, 60, 160, 170, and 180 min of the euglycemic/hyperinsulinemic clamp (EHC). We evaluated insulin sensitivity, body composition, and blood lipid profiles as well as fasting concentrations of CRP, TNF-α, and sTNF-R1.

Results: In fasting conditions, sTNF-R1 was negatively correlated with AcylG (r = −0.48, P < 0.001) levels. In addition, AcylG/TotG was associated negatively with sTNF-R1 (r = −0.44, P = 0.002) and positively with TNF-α (r = 0.38, P = 0.009) values. During the EHC, TotG (at all time points) and AcylG (at 60 and 160 min) values were significantly decreased from fasting concentrations. AcylG maximal reduction and area under the curve (AUC) values were correlated to sTNF-R1 (r = −0.35, P = 0.02 and r = −0.34, P = 0.02, respectively). Meanwhile, the AcylG/TotG AUC ratio was associated negatively with sTNF-R1 (r = −0.29, P < 0.05) and positively with TNF-α (r = 0.36, P = 0.02). Following adjustments for total adiposity, sTNF-R1 remained correlated with fasting and maximal reduction AcylG values. Similarly, AcylG/TotG ratios remained significantly correlated with sTNF-R1 and TNF-α. Importantly, 23% of the variation in sTNF-R1 was independently predicted by fasting AcylG.

Conclusion: These results are the first to suggest that both fasting and EHC-induced AcylG profiles are correlated with fasting values of sTNF-R1, a component of the TNF-α system. Thus, AcylG may act, at least in part, as one mediator of chronic inflammatory activity in human obesity.