Journal of clinical lipidology · 2017
Growth hormone activates hepatic and cerebral cholesterol metabolism in small-for-gestational age children without catch-up growth.
Клиническое исследованиеСтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Hirayama Satoshi, Nagasaka Hironori, Nakagawa Saori, Takuwa Mayuko, Nakacho Mariko, Yorifuji Tohru, Kondou Hiroki, Tsukahara Hirokazu, Morioka Ichiro, Ishida Akihito, Yamato Susumu, Miida Takashi
Аннотация
BACKGROUND: Growth hormone (GH) replacement therapy improves hypercholesterolemia in patients with GH deficiency, suggesting that GH modulates cholesterol metabolism.
OBJECTIVES: We examined GH effects on lipid profiles and cholesterol-related markers reflecting hepatic and cerebral cholesterol metabolism in small-for-gestational age (SGA) children without catch-up growth.
METHODS: This study examined SGA children without catch-up growth (n = 22) and healthy children (controls, n = 11). Based on parents' choice, 11 SGA children received GH at 0.23 to 0.25 mg/kg/d for 6 months, and at 0.34 to 0.36 mg/kg/d for the subsequent 6 months (GH (+) group). The other SGA children received no GH (GH (-) group, n = 11). We ascertained baseline and posttreatment lipid profiles and cholesterol-related markers reflecting hepatic and cerebral cholesterol metabolism.
RESULTS: Baseline lipid profiles of SGA children and controls were similar. Serum 24S-hydroxycholesterol (marker for cerebral cholesterol metabolism) concentration was 19% lower in SGA children than in controls (P < .05). Compared with baseline, the GH (+) group low-density lipoprotein-cholesterol concentration had decreased by 6.6% during 6 months and 8.8% during 12 months (P < .01), whereas the high-density lipoprotein-cholesterol concentration had increased by 1.7% (P = .07) and 3.3% (P < .01). Serum 7α-hydroxycholesterol (marker for hepatic cholesterol elimination) concentration had increased by 34% at 6 months and 35% at 12 months (P < .01). In addition, 24S-hydroxycholesterol increased by 25% and 26% (P < .001). No marker for cholesterol synthesis or absorption changed. The GH (-) group lipid profiles and oxysterols remained unchanged during the observation period.
CONCLUSION: GH activates hepatic and cerebral cholesterol metabolism in SGA children without catch-up growth.
OBJECTIVES: We examined GH effects on lipid profiles and cholesterol-related markers reflecting hepatic and cerebral cholesterol metabolism in small-for-gestational age (SGA) children without catch-up growth.
METHODS: This study examined SGA children without catch-up growth (n = 22) and healthy children (controls, n = 11). Based on parents' choice, 11 SGA children received GH at 0.23 to 0.25 mg/kg/d for 6 months, and at 0.34 to 0.36 mg/kg/d for the subsequent 6 months (GH (+) group). The other SGA children received no GH (GH (-) group, n = 11). We ascertained baseline and posttreatment lipid profiles and cholesterol-related markers reflecting hepatic and cerebral cholesterol metabolism.
RESULTS: Baseline lipid profiles of SGA children and controls were similar. Serum 24S-hydroxycholesterol (marker for cerebral cholesterol metabolism) concentration was 19% lower in SGA children than in controls (P < .05). Compared with baseline, the GH (+) group low-density lipoprotein-cholesterol concentration had decreased by 6.6% during 6 months and 8.8% during 12 months (P < .01), whereas the high-density lipoprotein-cholesterol concentration had increased by 1.7% (P = .07) and 3.3% (P < .01). Serum 7α-hydroxycholesterol (marker for hepatic cholesterol elimination) concentration had increased by 34% at 6 months and 35% at 12 months (P < .01). In addition, 24S-hydroxycholesterol increased by 25% and 26% (P < .001). No marker for cholesterol synthesis or absorption changed. The GH (-) group lipid profiles and oxysterols remained unchanged during the observation period.
CONCLUSION: GH activates hepatic and cerebral cholesterol metabolism in SGA children without catch-up growth.