title: Reduced growth hormone secretion in obesity is associated with smaller LDL and HDL particle size.
abstract: OBJECTIVE
  Reduced growth hormone (GH) secretion is observed in obesity and may contribute to increases in cardiovascular disease (CVD) risk. Lipoprotein characteristics including increased small dense low-density lipoprotein (LDL) particles are known independent risk factors for CVD. We hypothesized that reduced GH secretion in obesity would be associated with a more atherogenic lipid profile including increased small dense LDL particles.
  
  
  METHODS
  To evaluate this hypothesis, we studied 102 normal weight and obese men and women using standard GH stimulation testing to assess GH secretory capacity and performed comprehensive lipoprotein analyses including determination of lipoprotein particle size and subclass concentrations using proton NMR spectroscopy.
  
  
  RESULTS
  Obese subjects were stratified into reduced or sufficient GH secretion based on the median peak-stimulated GH (≤6·25 μg/l). Obese subjects with reduced GH secretion (n = 35) demonstrated a smaller mean LDL and HDL particle size in comparison to normal weight subjects (n = 33) or obese subjects with sufficient GH (n = 34) by ANOVA (P < 0·0001). Univariate analyses demonstrated peak-stimulated GH was positively associated with LDL (r = 0·50; P < 0·0001) and HDL (r = 0·57; P < 0·0001), but not VLDL (P = 0·06) particle size. Multivariate regression analysis controlling for age, gender, race, ethnicity, tobacco, use of lipid-lowering medication, BMI and HOMA demonstrated peak-stimulated GH remained significantly associated with LDL particle size (β = 0·01; P = 0·01; R(2) = 0·42; P < 0·0001 for overall model) and HDL particle size (β = 0·008; P = 0·001; R(2) = 0·44; P < 0·0001 for overall model).
  
  
  CONCLUSIONS
  These results suggest reduced peak-stimulated GH in obesity is independently associated with a more atherogenic lipoprotein profile defined in terms of particle size.
authors.affiliation: Program in Nutritional Metabolism and Neuroendocrine Unit, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA. hmakimura@partners.org
authors.forename: Hideo
authors.initials: H
authors.lastname: Makimura
authors.forename: Meghan N
authors.initials: MN
authors.lastname: Feldpausch
authors.forename: Takara L
authors.initials: TL
authors.lastname: Stanley
authors.forename: Noelle
authors.initials: N
authors.lastname: Sun
authors.forename: Steven K
authors.initials: SK
authors.lastname: Grinspoon
mesh_terms: D000328:Adult; D002318:Cardiovascular Diseases / Q000209:etiology; D053480:Cholesterol Ester Transfer Proteins / Q000097:blood; D005260:Female; D019382:Human Growth Hormone / Q000378:metabolism*; D006801:Humans; D008075:Lipoproteins, HDL / Q000737:chemistry*; D008077:Lipoproteins, LDL / Q000737:chemistry*; D008297:Male; D009765:Obesity / Q000150:complications / Q000378:metabolism*; D010316:Particle Size; D012044:Regression Analysis
chemical_list: D053480:Cholesterol Ester Transfer Proteins; D008075:Lipoproteins, HDL; D008077:Lipoproteins, LDL; D019382:Human Growth Hormone