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Comparative Analysis of Human Growth Hormone in Serum Using SPRi, Nano-SPRi and ELISA Assays
Published on: January 7, 2016
Effects of growth hormone (GH) administration on homocyst(e)ine levels in men with GH deficiency: a randomized
G Sesmilo1, B M Biller, J Llevadot
1Department of Laboratory Medicine, Children's Hospital and Harvard Medical School, Boston, 02114, USA.
Insights
Growth hormone (GH) replacement therapy in men with adult-onset GH deficiency significantly reduced fasting homocyst(e)ine levels. This finding suggests a potential mechanism for GH’s role in mitigating cardiovascular risk and atherosclerosis.
Area of Science:
- Endocrinology
- Cardiovascular Medicine
- Metabolic Research
Background:
- Growth hormone (GH) deficiency is linked to increased cardiovascular mortality and atherosclerosis.
- Elevated serum homocyst(e)ine is a known cardiovascular risk factor.
- The impact of GH replacement on homocyst(e)ine levels has not been previously studied.
Purpose of the Study:
- To investigate the effect of GH replacement therapy on fasting homocyst(e)inemia in men with adult-onset GH deficiency.
- To explore potential correlations between homocyst(e)ine changes and other metabolic markers.
Main Methods:
- A randomized, single-blind, placebo-controlled trial involving 40 men with adult-onset GH deficiency.
- Participants received either GH or placebo for 18 months, with GH dosage adjusted based on serum insulin-like growth factor I (IGF-I) levels.
- Fasting serum homocyst(e)ine, folate, vitamin B12, and total T(3) were measured at baseline, 6, and 18 months.
Main Results:
- Homocyst(e)ine levels significantly decreased in the GH-treated group compared to the placebo group (net difference: -1.2 micromol/L, P=0.047).
- GH treatment led to a significant increase in total T(3) levels.
- Changes in homocyst(e)ine were negatively correlated with changes in IGF-I levels.
Conclusions:
- GH replacement therapy effectively reduces fasting homocyst(e)ine levels in men with adult-onset GH deficiency.
- This reduction in homocyst(e)ine may contribute to the observed benefits of GH replacement in modulating atherosclerosis and cardiovascular risk.
Abstract:
GH deficiency is associated with increased cardiovascular mortality and early manifestations of atherosclerosis. Elevated serum homocyst(e)ine levels have been found to be associated with increased cardiovascular risk. The effect of GH replacement on homocyst(e)ine has not been investigated to date. We evaluated the effect of GH replacement on fasting homocyst(e)inemia in a group of men with adult-onset GH deficiency in a randomized, single blind, placebo-controlled trial. Forty men with adult-onset GH deficiency were randomized to GH or placebo for 18 months, with dose adjustments made according to serum insulin-like growth factor I (IGF-I) levels. Fasting serum homocyst(e)ine, folate, vitamin B12, and total T(3) levels were determined at baseline and 6 and 18 months. Anthropometry, IGF-I levels, insulin, and glucose were measured at 1, 3, 6, 12, and 18 months. Nutritional assessment, body composition, total T(4), thyroid hormone binding index, and free T(4) index were assessed every 6 months. Homocyst(e)ine decreased in the GH-treated group compared with that in the placebo group (net difference, -1.2 +/- 0.6 micromol/L; confidence interval, -2.4, -0.02 micromol/L; P = 0.047). Homocyst(e)ine at baseline was negatively correlated with plasma levels of folate (r = -0.41; P = 0.0087). Total T(3) increased in the GH-treated group vs. that in the placebo group (net difference, 0.17 +/- 0.046 ng/dL; confidence interval, 0.071, 0.26 nmol/L; P = 0.0012). Folate and vitamin B12 levels did not significantly change between groups. Changes in homocyst(e)ine were negatively correlated with changes in IGF-I. For each 1 nmol/L increase in IGF-I, homocyst(e)ine decreased by 0.04 +/- 0.02 micromol/L (P = 0.029). In contrast, changes in homocyst(e)ine did not correlate with changes in folate, vitamin B12, total T(3), C-reactive protein, interleukin-6, or insulin levels. This study shows that GH replacement decreases fasting homocyst(e)ine levels compared with placebo. This may be one of the mechanisms involved in the putative modulation of atherosclerosis and cardiovascular risk by GH replacement.
