Rosenbaum M, Gertner J M, Gidfar N, Hirsch J, Leibel R L
Division of Pediatric Endocrinology, New York Hospital-Cornell University Medical Center, New York.
J Clin Endocrinol Metab. 1992 Jul;75(1):151-6. doi: 10.1210/jcem.75.1.1619004.
Chronic administration of exogenous GH to GH-deficient children is associated with a selective depletion of the abdominal sc fat depot and a resultant relative increase in gluteal, relative to abdominal, adipocyte lipid content. In GH-deficient children, the degree of this change in relative lipid content per adipocyte appears to be correlated with decreases in sensitivity of abdominal subcutaneous fat to the antilipolytic action of insulin. We studied abdominal and gluteal sc adipose tissue from 10 children with short stature (height less than 5% ile, growth velocity less than 5 cm/yr, bone age delayed at least 2 yr), who were not GH deficient based upon provocative testing (non-GH-deficient short stature) 1) before beginning and 2) after 3 months of therapy with exogenous GH (Humatrope, 0.1 mg/kg sc 3 times/week). In abdominal and gluteal adipocytes, we measured lipid content, rates of reesterification of fatty acids released by ongoing lipolysis and rates of in vitro lipolysis and lipogenesis in response to insulin, adenosine, and various adrenoreceptor agonists. These biochemical measures were correlated with measures of statural growth and adipose tissue distribution in each subject. We found that GH therapy was associated with a significant reduction in abdominal adipocyte size (0.48 microgram +/- 0.08 lipid per cell prior to therapy vs. 0.43 microgram +/- 0.08 lipid per cell after therapy, P less than 0.05) and a significant increase in responsiveness of gluteal sc adipose tissue to the lipogenic actions of insulin. The significant correlations of changes in abdominal adipocyte volume with changes in regional adipose tissue insulin sensitivity that were noted in GH-deficient children were not noted in this subject population, perhaps due to effects of endogenous GH on pretreatment insulin responsiveness of adipose tissue. These data reaffirm that GH has site-specific effects on regional adipose tissue depots.
对生长激素缺乏的儿童长期给予外源性生长激素，会导致腹部皮下脂肪储存选择性减少，从而使臀肌脂肪细胞脂质含量相对于腹部脂肪细胞脂质含量相对增加。在生长激素缺乏的儿童中，每个脂肪细胞相对脂质含量的这种变化程度似乎与腹部皮下脂肪对胰岛素抗脂解作用敏感性的降低相关。我们研究了10名身材矮小儿童（身高低于第5百分位，生长速度低于每年5厘米，骨龄至少延迟2年）的腹部和臀部皮下脂肪组织，这些儿童经激发试验并非生长激素缺乏（非生长激素缺乏性身材矮小）：1）在开始治疗前；2）在用外源性生长激素（健豪宁，0.1毫克/千克皮下注射，每周3次）治疗3个月后。在腹部和臀部脂肪细胞中，我们测量了脂质含量、正在进行的脂解所释放脂肪酸的再酯化率以及体外脂解和脂肪生成率，这些是对胰岛素、腺苷和各种肾上腺素能受体激动剂的反应。这些生化指标与每个受试者的身高增长和脂肪组织分布指标相关。我们发现，生长激素治疗与腹部脂肪细胞大小显著减小有关（治疗前每个细胞脂质含量为0.48微克±0.08，治疗后为0.43微克±0.08，P<0.05），并且臀部皮下脂肪组织对胰岛素脂肪生成作用的反应性显著增加。在生长激素缺乏的儿童中所观察到的腹部脂肪细胞体积变化与局部脂肪组织胰岛素敏感性变化之间的显著相关性，在该受试人群中未观察到，这可能是由于内源性生长激素对治疗前脂肪组织胰岛素反应性的影响。这些数据再次证实生长激素对局部脂肪组织储存具有部位特异性作用。
