Metabolic Parameters and Adipokine Profile in Growth Hormone Deficient (GHD) Children Before and After 12-Month GH Treatment

Abstract

It is a common knowledge that GH exhibits a large number of metabolic effects, involving lipid and glucose homeostasis. The aim of the study was to investigate the effect of one year GH therapy on metabolic parameters and adipokines in GH deficient (GHD) children. Sixteen prepubertal children (11 M and 5 F) with complete GHD (age range: 3.4-14.7 years) and 20 (13 M and 7 F) age and sex-matched healthy children (age range: 4.6-12.3 years) were studied. Blood was collected from patients before starting GH therapy (0.025 mg/kg/day) and one year later, and from healthy children to measure adiponectin, leptin, osteoprotegerin, resistin, interleukin (IL)-6, tumor necrosis factor (TNF)-α levels, and other glucose and lipid metabolism parameters. Adiponectin and resistin levels were significantly higher (49980 ng/ml vs. 14790 ng/ml and 11.0 pg/ml vs. 6.3, respectively) in GHD children before GH therapy than in controls. Serum IGF-I levels (p=0.0001) and height SDS (p<0.0001) significantly increased after 12 months' of GH therapy. There was a loss of body fat reflected by a significant decline in tricep (p=0.0003) and subscapular skinfold thickness SDS (p=0.0023). After 12 months, there was a significant rise in insulin (p=0.0052) and leptin levels (p=0.0048) and a significant decrease in resistin (p=0.0312) and TNF-α (p=0.0137). We observed that lipid and glucose metabolisms are only slightly affected in GHD children. Growth hormone replacement therapy affects some factors, such as leptin, resistin and fat mass, suggesting that also in children, GH treatment has a role in the regulation of factors secreted by adipose tissue.

Resistin, visfatin, leptin and omentin are differently related to hormonal and metabolic parameters in growth hormone-deficient children

“…Our data are in agreement with some studies that have documented that GH treatment does not seem able to strongly modify resistin levels in GHD adults [10,20], although we found a trend to an increase in resistin levels after 12 months, though not statistically significant. Partially in line with our results, Nozue et al [21] demonstrated a rise in resistin after short-term GH therapy in GHD children, while López-Siguero et al [12] showed a decline in resistin at 6 months of GH treatment and these data are in line with those of Meazza et al [19] who showed a decrease in resistin levels. However, despite the lack of a statistically significant change, the trend to an increase in resistin in our patients during GH treatment is concomitant with a significant reduction in insulin sensitivity, as demonstrated by the decline in QUICKI and ISI Matsuda, in line with previous studies.…”

“…Indeed, a possible mediator of the GH-modulated insulin sensitivity may be resistin, which has been shown to be linked to obesity and insulin resistance [18]. Higher resistin levels in untreated GHD children than controls have already been documented [19], while the effect of GH treatment is controversial. Our data are in agreement with some studies that have documented that GH treatment does not seem able to strongly modify resistin levels in GHD adults [10,20], although we found a trend to an increase in resistin levels after 12 months, though not statistically significant.…”

Response to IGF-1 Generation Test in Short Prepubertal Children Born Very Preterm or at Term

“…Some studies have reported a decrease in leptin levels in short children with [45,46] and without [42] GH deficiency after 1 year of GH therapy. Conversely, Meazza et al [47] have detected a significant increase in leptin levels after 1 year of GH treatment in children with GH deficiency.…”

Developments in our understanding of the effects of growth hormone on white adipose tissue from mice: implications to the clinic

“…Importantly, it results in an overall reduction of fat mass, including a shift in adipocyte volume and size toward normal [78, 79]. Levels of insulin and adipokines are partly normalized, and especially in adult GHD, lipid metabolism is improved [39, 80]. Patients with LS show clinical manifestations that are similar, although not identical, to GHD.…”