Ghrelin secretion is modulated in a nutrient- and gender-specific manner.
BACKGROUND
Ghrelin is a potent GH secretagogue that also plays an important role in appetite and weight regulation. Ghrelin increases hunger and food intake, and its levels decrease after a standard meal or glucose.


OBJECTIVE
To examine the effects of standard oral glucose, lipid and protein loads on ghrelin levels, investigating the possibility that these responses may be modulated by several anthropometric and metabolic factors.


METHODS
There were 24 adult nondiabetic subjects (13 men/11 women; mean age 55.3 +/- 2.9 years, range 26-74 years). Each participant underwent one or more of the following nutrient loads: (i) a standard oral glucose (75 g) load (n = 18); (ii) an oral lipid load (40 g, with 24 g saturated fat; n = 13); (iii) an oral protein load (40 g; n = 11).


RESULTS
Fasting ghrelin levels were negatively related to body mass index (BMI; r =-0.47; P = 0.02), waist circumference (r = -0.58; P = 0.0028), waist/hip ratio (r = -0.56; P = 0.0046), fasting insulin (r = -0.44, P = 0.03), and homeostasis model assessment insulin resistance index (HOMA-R; r = -0.43, P = 0.034). Glucose load induced a decrease in ghrelin levels (P < 0.0001), and this response was modulated by sex (P < 0.0001), in that levels were significantly higher in females. The presence of obesity affected ghrelin response to glucose (< 0.0217), in that log-transformed ghrelin levels started to increase back to baseline after its initial decline earlier in obese than in lean subjects. Ghrelin levels after a glucose load were lower over time in subjects with more pronounced insulin resistance (P < 0.0001). Similarly, ghrelin levels decreased significantly following the lipid meal (P = 0.035), and were modulated by HOMA-R (P = 0.027) and gender (P = 0.029). Protein did not affect ghrelin levels.


CONCLUSIONS
This study demonstrates that ghrelin levels respond in a different manner to glucose, lipid and protein loads, and are subject to modulation according to gender, obesity and insulin sensitivity.
Greenman
Yona
Y
Institute of Endocrinology, Metabolism and Hypertension, Tel Aviv-Sourasky Medical Center, Sackler School of Medicine Tel Aviv University, Tel Aviv, Israel. greenman@tasmc.health.gov.il
Golani
Nehama
N
Gilad
Susan
S
Yaron
Mariana
M
Limor
Rona
R
Stern
Naftali
N
D000328:Adult; D000368:Aged; D001069:Appetite Regulation; D001823:Body Composition; D015992:Body Mass Index; D004041:Dietary Fats / Q000008:administration & dosage; D004044:Dietary Proteins / Q000008:administration & dosage; D005260:Female; D054439:Ghrelin; D005947:Glucose / Q000008:administration & dosage; D006801:Humans; D007328:Insulin / Q000097:blood; D008297:Male; D008875:Middle Aged; D009747:Nutritional Physiological Phenomena; D036361:Peptide Hormones / Q000097:blood*; D019518:Postprandial Period; D012737:Sex Factors
D004041:Dietary Fats; D004044:Dietary Proteins; D054439:Ghrelin; D007328:Insulin; D036361:Peptide Hormones; D005947:Glucose