GH peak response to GHRH-arginine: relationship to insulin resistance and other cardiovascular risk factors in a population of adults aged 50-90.
OBJECTIVE
To assess the GH response to GHRH-arginine in apparently healthy adults in relation to cardiovascular risk factors.


METHODS
Cross-sectional.


METHODS
Eighty-six male and female volunteers aged 50-90.


METHODS
GH peak response to GHRH-arginine and cardiovascular risk factors, including obesity, insulin resistance, low levels of high density lipoprotein (HDL) cholesterol, elevated triglycerides, and hypertension. The primary outcome measurement was GH response to GHRH-arginine. The relationship between GH peak responses and cardiovascular risk factors was determined after data collection.


RESULTS
GH peaks were highly variable, ranging from 2.3 to 185 microg/l (14% with GH peaks < 9 microg/l). An increasing number of cardiovascular risk factors were associated with a lower mean GH peak (P < 0.0001). By univariate analysis, fasting glucose, insulin, body mass index (BMI), HDL cholesterol and triglycerides were significantly associated with GH peak (all P < 0.0001). Multiple regression analysis revealed that fasting glucose, fasting insulin, BMI, triglycerides and sex accounted for 54% of GH peak variability. The role of abdominal fat as it relates to GH peak was explored in a subset of 45 subjects. Trunk fat and abdominal subregion fat measured by dual energy X-ray absorptiometry (DXA) were inversely related to GH peak (P < 0.008 and 0.001, respectively). Analysis of this subgroup by multiple regression revealed that subregion abdominal fat became the significant obesity-related determinant of GH peak, but still lagged behind fasting insulin and glucose.


CONCLUSIONS
GH response to secretagogues was highly variable in apparently healthy adults aged 50-90 years. Peak GH was significantly related to fasting glucose, insulin, BMI, HDL cholesterol, triglycerides, trunk fat and abdominal subregion fat, with fasting glucose ranking first by multiple regression analysis. There was a strong relationship between cardiovascular risk factors and low GH, with individual risk factors being additive. Although these data do not differentiate between low GH being a cause or an effect of these cardiovascular risk factors, they indicate that the relationship between low GH and increased cardiovascular risk may be physiologically important in the absence of pituitary disease.
Carmichael
John D
JD
Neuroendocrine Unit, Division of Endocrinology, General Clinical Research Center, New York University School of Medicine ,New York, NY, USA.
Danoff
Ann
A
Milani
Daniela
D
Roubenoff
Ronenn
R
Lesser
Martin L
ML
Livote
Elayne
E
Reitz
Richard E
RE
Ferris
Steven
S
Kleinberg
David L
DL
D015502:Absorptiometry, Photon; D000368:Aged; D000369:Aged, 80 and over; D001120:Arginine; D001786:Blood Glucose / Q000032:analysis; D001823:Body Composition; D015992:Body Mass Index; D002318:Cardiovascular Diseases / Q000209:etiology; D003430:Cross-Sectional Studies; D005260:Female; D013006:Growth Hormone / Q000097:blood*; D013007:Growth Hormone-Releasing Hormone; D006706:Homeostasis; D006801:Humans; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance; D007334:Insulin-Like Growth Factor I / Q000032:analysis; D008297:Male; D008875:Middle Aged; D012044:Regression Analysis; D012307:Risk Factors
D001786:Blood Glucose; D007328:Insulin; D007334:Insulin-Like Growth Factor I; D013006:Growth Hormone; D013007:Growth Hormone-Releasing Hormone; D001120:Arginine