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Division of Endocrinology, Diabetes, and Clinical Nutrition (J.Q.P.), Oregon Health & Science University, Portland, Oregon 97201; and University of Washington (D.S.W., P.B., D.E.C.), Veterans Affairs Puget Sound Health Care System and Harborview Medical Center, Seattle, Washington 98108
Address all correspondence and requests for reprints to: Jonathan Q. Purnell, M.D., Oregon Health & Science University, Division of Endocrinology, Diabetes, and Clinical Nutrition, L607, 3181 SW Sam Jackson Park Road, Portland, Oregon 97201. E-mail: purnellj{at}ohsu.edu.
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Abstract |
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Introduction |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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Unlike other gut peptides, which are secreted in response to meals and contribute to postprandial satiety, ghrelin levels increase before meals, stimulate appetite, and decrease after food intake (6, 7, 8). In addition to having a potential role in meal initiation (7), ghrelin may function as an adiposity signal that contributes to weight regain in postobese subjects, as evidenced by the increase in circulating ghrelin levels that accompanies voluntary or disease-induced weight loss (6, 9, 10, 11).
Several studies have reported the relationships between overnight fasting ghrelin levels and parameters of body weight and glucose metabolism. Ghrelin secretion throughout the day is, however, highly variable, and it is important to establish that one time point accurately reflects daily ghrelin exposure. Also, if ghrelin functions as a long-term adiposity signal, the parameter(s) reflecting body composition—either directly (body fat amount or distribution) or indirectly (glucose or lipid metabolism)—that explain variations in ghrelin levels among individuals are unknown. In this study, we examine the associations between ghrelin levels and these parameters, including body composition, fat distribution, age, leptin, insulin, insulin sensitivity, lipids, and hormonal status in women. In addition, 24-h profiles of ghrelin and cortisol levels were compared to determine whether physiological variations in ghrelin levels are associated with similar changes in cortisol levels, as suggested by the observation that ghrelin stimulates ACTH and cortisol secretion in humans.
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Subjects and Methods |
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Subjects were recruited using local newspaper and campus advertising. All were at least 18 yr old and had stable body weight for at least 3 months. Exclusion criteria included chronic medical or psychiatric illness, pregnancy, tobacco use, substance abuse, alcohol consumption of more than two drinks per day, and aerobic exercise greater than 30 min three times per week. The Oregon Health & Science University (OHSU) and the University of Washington (UW) Human Subjects Review Committees approved all procedures and protocols, and written informed consent was obtained before enrollment.
Subjects were admitted to the University of Washington General Clinical Research Center after an overnight fast. An iv catheter was placed for blood drawing, and after a 15-min rest period, baseline blood samples were withdrawn for lipid measurements and post-heparin (60 U/kg) lipase activity. After these studies, beginning at 0800 h, blood was collected into EDTA-containing tubes every 30 min until 2100 h, then hourly until 0800 h the next morning (24-h total). Samples were stored at 4 C during the collection period, after which plasma was stored at -80 C. Breakfast, lunch, and dinner were served at 0800, 1200, and 1730 h, respectively.
Lipids and post-heparin lipase activities
Cholesterol and triglyceride levels were determined by standardized methods at the Northwest Lipid Research Laboratories (12). Low- density lipoprotein (LDL) buoyancy (relative floatation rate or Rf) was determined by nonequilibrium density gradient ultracentrifugation as previously described (13). Lipoprotein lipase (LPL) and hepatic lipase (HL) activities were determined as previously described (14). The intraassay coefficients of variation of this assay are 7% for LPL and 6% for HL; the interassay coefficients of variation are 8% for LPL and 10% for HL.
Body composition
Body composition was quantified in 54 subjects by dual energy x-ray absorptiometry scan. Intraabdominal fat (IAF) and sc fat (SQF) were quantified by a single, blinded observer in 39 subjects using a single CT scan image obtained at the level of the umbilicus (15). Fat-cell volume (microliters of triglyceride per cell) was calculated using Goldrick’s equation (16) from the measured diameters of 400 adipocytes taken from an aspiration fat biopsy of the posterior-superior iliac crest region.
Plasma chemistries
Insulin levels were determined in duplicate using a modification of a double-antibody RIA (17), and glucose concentrations were determined in triplicate using the glucose oxidase method. Immunoreactive ghrelin levels were assessed in duplicate with a commercial RIA that recognizes both acylated and des-acyl forms (Phoenix Pharmaceuticals, Belmont, CA). Although only acylated ghrelin is bioactive (18), levels of total ghrelin are a good surrogate for those of acylated ghrelin because the ratio of the two remains constant under a wide variety of conditions (19, 20). Leptin was measured using a commercial RIA (Linco Research, St. Charles, MO). Cortisol levels were measured in duplicate by the OHSU General Clinical Research Center Core Laboratory using a two-site chemiluminescent assay (Nichols Institute, San Juan Capistrano, CA). Assay sensitivity was 0.8 mg/dl, and the intra- and interassay coefficients of variation were less than 8% for the cortisol levels measured in the study.
Statistical analysis
AUC (area under the curve) was calculated using the trapezoidal method. Insulin sensitivity was estimated by the quantitative insulin sensitivity check index [QUICKI = 1/{log(fasting insulin) + log(fasting glucose)}] (21). Triglyceride and QUICKI results were log-transformed before statistical testing. Comparisons between groups were analyzed using the t test when data followed normal distributions or by a rank sum test (Mann-Whitney U test) if data were not normally distributed. One-way ANOVA was used to test for significant differences among more than two groups. Linear relationships between variables were tested by correlational analysis (Pearson Product Moment) and linear regression.
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Results |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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In the subset of subjects (n = 31) who underwent 24-h blood sampling, 0800 h ghrelin level correlated strongly with daily AUC ghrelin (r = 0.89; P < 0.001) (Fig. 1). Because of this high degree of correlation, 0800 h ghrelin levels available from the entire cohort were used in the analyses below.
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Ghrelin levels correlated positively with age and negatively with body weight and BMI (Table 2 and Fig. 2). Of the measured parameters of body composition, ghrelin levels correlated negatively with the amount of SQF and fat-cell size, but did not significantly correlate with percentage fat, fat mass, lean mass, IAF, or leptin levels (Table 2 and Fig. 2).
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Ghrelin levels correlated negatively with fasting insulin levels and positively with the insulin sensitivity estimated by QUICKI (Table 3 and Fig. 2
). The relationship between the meal-related stimulation of insulin and suppression of ghrelin was also tested in 16 subjects in whom levels of both hormones were available for analysis (Fig. 3). Using data from timed samples beginning 30 min before each meal (breakfast, lunch, and dinner) and continuing for 2 h after the meal, the postmeal rise (nadir to peak) in insulin was associated with the fall (peak to nadir) in ghrelin levels (r = 0.39; P < 0.05). The 2-h postmeal cut-off was chosen for this analysis because previous studies have shown maximal suppression for ghrelin to occur within this time frame (7, 11).
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and Fig. 2). An inverse association between ghrelin levels and HL activity reached borderline significance (P = 0.07). Multiple linear regression analysis
Because many of these parameters correlate with one another (e.g. BMI, SQF, insulin levels, etc.), multiple linear regression analysis was used to determine independent associations with ghrelin levels. Including the variables from correlational analysis that were significantly associated with 0800 h ghrelin levels explained 32% of the variance in ghrelin levels (Table 4). None of the variables, however, were independently associated with 0800 h ghrelin.
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Ghrelin, gender, and menopausal status
Compared with men, women had higher percentage body fat (mean ± SD, 43 ± 7 vs. 28 ± 12%, women vs. men; P < 0.001) and HDL cholesterol levels (48 ± 11 vs. 40 ± 11 mg/dl, women vs. men; P = 0.001), whereas no significant differences between genders were found for age (45 ± 12 vs. 41 ± 11, females vs. males; P = 0.17), BMI (31 ± 6 vs. 35 ± 11 kg/m2; P = 0.21), insulin (15 ± 7 vs. 15 ± 10 µU/ml; P = 0.98), insulin sensitivity by QUICKI (0.33 ± 3 vs. 0.34 ± 5; P = 0.24), and ghrelin (417 ± 247 vs. 362 ± 290; P = 0.19). After adjustment for gender-based differences in HDL cholesterol levels, ghrelin levels agreed even more closely between women and men (394 ± 223 vs. 404 ± 290; P = 0.89). Ghrelin levels were not different among the 19 premenopausal (382 ± 218 pg/ml), the nine postmenopausal women (440 ± 317 pg/ml), and the 11 postmenopausal women taking hormone replacement therapy (458 ± 249 pg/ml) (P = 0.70 by one-way ANOVA).
Ghrelin and 24-h cortisol levels
Fasting 0800 h ghrelin levels were not associated with 24-h AUC cortisol levels (r = 0.14; P = 0.28), and no apparent relationship could be demonstrated between the 24-h profiles of these two hormones, with ghrelin levels showing meal-related suppression, whereas cortisol levels followed a typical circadian pattern (Fig. 4).
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Discussion |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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Published studies of ghrelin levels have relied primarily on single samples obtained after an overnight fast. However, ghrelin levels are strongly affected by food consumption and are quite variable during the day; therefore, a single fasting morning ghrelin level needs to be validated before it is used as a surrogate for the total daily exposure to ghrelin. We have previously shown that a single fasting blood sample taken at 0600 h or at the time of a postmeal trough correlated well with AUC ghrelin in a small number of subjects (n = 10) (7). However, 0800 h is a more common time for sampling in many studies. In the present study, therefore, we increased the number of subjects examined, included lean and obese individuals, and found that a single fasting 0800 h ghrelin level correlated well with the 24-h AUC value (r = 0.89; P < 0.001).
Using this 0800 h ghrelin level and detailed subject phenotyping, we confirmed previous findings of significant inverse relationships between ghrelin levels and both BMI (22) and fat-cell size (23), and also found a similar relationship between ghrelin and SQF. We found no relationship of ghrelin to percentage body fat, total fat mass, lean mass, IAF, or leptin levels. On multiple linear regression analysis, the significant inverse relationships between ghrelin and fat-cell size or SQF were not found to be independent of BMI. Therefore, our data suggest that of the multiple parameters of body composition studied, ghrelin levels best reflect body weight rather than specific amounts of fat or body fat distribution.
It is not known what mechanism causes ghrelin levels to reflect body weight and to be regulated in the manner of an adiposity signal, as suggested by studies in which ghrelin levels rise after diet-induced weight loss (11). Candidate regulators that are highly associated with body weight include several parameters of glucose and lipid metabolism. In the present study, ghrelin levels correlated with insulin (negatively), insulin sensitivity (positively), HDL cholesterol (positively), and LDL peak particle buoyancy (positively). In nondiabetic individuals, lower insulin levels often reflect greater insulin sensitivity, and given the cross-sectional design of the present study, the relative or independent contribution of these insulin measurements to ghrelin levels cannot be determined. Insulin, however, has been shown to play a role in the long-term regulation of body adiposity (24). In conjunction with prior observations implicating insulin in the regulation of ghrelin (25), the present findings identify insulin as a leading candidate for a long-term mediator of ghrelin responses to weight change.
Our data also show an association between the acute, meal-related increase in insulin levels with the decrease in ghrelin levels. Our data are cross-sectional, however, and do not establish a causative role for physiological meal-related insulin secretion to suppress ghrelin. Although studies using hyperinsulinemic-euglycemic clamps have demonstrated that ghrelin levels are suppressed during insulin infusions (25, 26, 27), other meal-related hormones are associated with ghrelin suppression, including glucagon-like peptide 1 (28). Therefore, the precise role of insulin in the suppression of ghrelin during nutrient ingestion in humans has yet to be established.
HDL cholesterol may seem an unlikely variable to be associated with ghrelin levels, but a recent study demonstrated that ghrelin binds to HDL particles and is found concentrated in HDL-containing lipid fractions from human plasma (29). Although the assay used in the present study measures total ghrelin (bound, unbound, acylated, and desacylated), the finding of a positive association of ghrelin levels and HDL cholesterol supports the possible role of HDL particles as circulating transporters of ghrelin (29). The known associations between HDL cholesterol, LDL buoyancy, and HL activity most likely explain the additional findings in the present study of a significant correlation between ghrelin and LDL peak particle density and the borderline significant correlation with HL activity. Therefore, studies in which an intervention is shown to affect ghrelin levels should include measurements of insulin, insulin sensitivity, and HDL cholesterol, to exclude the possibility that changes in these variables independently influenced ghrelin levels.
Examples of the confounding effect of these associations can be found in the relationships we report here between ghrelin, aging, and BMI. In the present data set, aging was not associated with body weight, insulin, or insulin sensitivity; but it was significantly (positively) correlated with HDL cholesterol. On multiple linear regression with HDL cholesterol included, age was no longer independently associated with ghrelin levels. Likewise, previous studies have reported that ghrelin levels are associated with BMI, insulin, and insulin resistance (23, 30), but did not study the independence of these variables to predict ghrelin levels. In our study, BMI was not independently associated with ghrelin levels after including insulin levels or insulin sensitivity in multiple linear regression analyses. These findings further support the hypothesis that insulin signaling may mediate the relationship between BMI and ghrelin levels.
We confirm previous reports showing no difference in ghrelin levels between men and women (22). Adjustment for gender-based HDL cholesterol differences further diminished any small difference between sexes. This lack of difference in ghrelin levels between men and women supports our conclusion that ghrelin levels vary as a function of body weight rather than percentage fat, because the women in our study had significantly higher percentage body fat than did the men. We also report here for the first time that ghrelin levels are not different in women according to menopausal or hormone-replacement status, a finding that suggests ghrelin levels are not physiologically regulated by estrogen in women.
Finally, based on studies demonstrating that pharmacological doses of ghrelin stimulate the hypothalamic-pituitary-adrenal axis in humans (1, 2), we sought to determine whether physiological changes in ghrelin levels during the day varied with, or predicted, measured cortisol levels. We found, however, that daily ghrelin and cortisol (either in total amount by AUC or secretion patterns) were not apparently related.
By performing more extensive phenotyping of body composition and parameters of glucose and lipid metabolism in a single cohort, we sought to characterize better those variables that best predict ghrelin levels. Ghrelin levels are inversely related to BMI but do not correlate with body composition or abdominal fat distribution as measured by computed tomography. Independent relationships between ghrelin, insulin, and HDL, however, explain the univariate associations between ghrelin, BMI, and age. Insulin signaling is a leading candidate mechanism governing the inverse relationship between body weight and ghrelin. Gender, postmenopausal status (including hormonal replacement), and changes in cortisol levels within the physiological range do not appear to influence ghrelin levels in humans. Studies of ghrelin levels should include measurements of insulin and HDL cholesterol to avoid confounding effects of changes in these variables on ghrelin levels.
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Acknowledgments |
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Footnotes |
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Abbreviations: AUC, Area under the curve; BMI, body mass index; HDL, high-density lipoprotein; HL, hepatic lipase; IAF, intra-abdominal fat; LDL, low-density lipoprotein; LPL, lipoprotein lipase; QUICKI, quantitative insulin sensitivity check index; SQF, sc fat.
Received March 25, 2003.
Accepted August 28, 2003.
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G. Marchesini, G. Bianchi, P. Lucidi, N. Villanova, M. Zoli, and P. De Feo Plasma Ghrelin Concentrations, Food Intake, and Anorexia in Liver Failure J. Clin. Endocrinol. Metab., May 1, 2004; 89(5): 2136 - 2141. [Abstract] [Full Text] [PDF]
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