Key result
Adult-onset growth hormone deficiency was associated with significantly increased fasting (0.31 vs 0.18 mmol/L) and postprandial RLP-C levels compared to healthy controls.
Why the study?
Does an oral fat load induce a greater postprandial inflammatory response and higher RLP-C levels in AGHD patients compared to healthy controls?
Case-Control (n=20)
Does an oral fat load induce a greater postprandial inflammatory response and higher RLP-C levels in AGHD patients compared to healthy controls?
Absolute Event Rate: 0.31% vs 0.18%
Increased postprandial RLP-C levels in adult-onset growth hormone deficiency are associated with an inflammatory response, potentially explaining their increased susceptibility to premature atherosclerosis.
May link AGHD to atherosclerosis via remnant lipoproteins; hypothesis-generating for GH therapy effects on postprandial lipids.
Increased cardiovascular mortality due to premature atherosclerosis is a clinical feature in the adult-onset GH deficiency (AGHD) syndrome. Inflammation is a key feature in atherogenesis and may be triggered by postprandial lipoprotein remnants. We hypothesized that increased postprandial lipoprotein remnant levels in AGHD may be associated with an inflammatory response. In this case-control study, 10 AGHD patients [6 males and 4 females; age, 48 +/- 9 yr; body mass index (BMI), 26.9 +/- 2.6 kg/m(2)] and 10 healthy control subjects (matched for age, BMI, gender, baseline lipid levels, and apolipoprotein E genotype) were included. They all ingested an oral fat load. Fasting and postprandial levels of plasma remnant-like particle-cholesterol (RLP-C; 0.31 +/- 0.13 mmol/liter and 4.14 +/- 1.37 mmol/liter.h in GHD; 0.18 +/- 0.06 mmol/liter and 2.56 +/- 1.02 mmol/liter.h in controls, respectively) were significantly increased in AGHD patients compared with control subjects. The median inflammatory cytokines, IL-6 and TNF-alpha, were higher in the fasting [3.9 (range, 3.1-11.9) pg/ml and 6.8 (range, 2.5-27.6) pg/ml, respectively] and postprandial [151.7 (range, 87.0-294.3) pg/ml.24 h and 289.9 (range, 87.5-617.6) pg/ml.24 h, respectively] states in AGHD than in controls [fasting, 0.9 (range, 0.2-5.2) pg/ml and 2.8 (range, 2.5-5.7) pg/ml; and postprandial, 54.5 (range, 11.50-126.5) pg/ml.24 h and 118.3 (range, 81.2-243.1) pg/ml.24 h, respectively]. In addition, postprandial profile of RLP-C and IL-6 in AGHD and in the total group were significantly associated (r(2) = 0.44, P < 0.05; and r(2) = 0.38, P < 0.01, respectively). In conclusion, the increased postprandial RLP-C level in GHD is associated with an inflammatory response that may result in increased susceptibility for premature atherosclerosis.
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Twickler et al. (2003) conducted a case-control in Adult-onset growth hormone deficiency (AGHD) (n=20). Adult-onset growth hormone deficiency vs. Healthy control subjects was evaluated on Fasting plasma remnant-like particle-cholesterol (RLP-C) in mmol/liter. Adult-onset growth hormone deficiency was associated with significantly increased fasting (0.31 vs 0.18 mmol/L) and postprandial RLP-C levels compared to healthy controls.
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