The Journal of clinical endocrinology and metabolism · 2025
Growth Hormone Promotes Hepatic Triglyceride Export in Humans.
СтатьяНазвание и аннотация: Перевод пока не подготовлен
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.
Baumgartner Clemens, Metz Matthäus, Beghini Marianna, Pfleger Lorenz, Tosin Anna, Koldyka Oliver, Beiglböck Hannes, Fellinger Paul, Vila Greisa, Luger Anton, Kautzky-Willer Alexandra, Freudenthaler Angelika, Baumgartner-Parzer Sabina, Stangl Herbert, Krssak Martin, Carli Fabrizia, Infelise Patrizia, Gastaldelli Amalia, Scherer Thomas, Krebs Michael, Wolf Peter
Аннотация
CONTEXT: Growth hormone (GH) reduces intrahepatic lipids (IHL) according to investigations in healthy volunteers and patients with acromegaly, a disease characterized by long-term GH excess.
OBJECTIVE: This study investigated underlying antisteatotic pathways stimulated by short-term modulation of GH action.
METHODS: Ten healthy male volunteers (26 ± 5 years, body mass index [BMI] 23 ± 3.4 kg/m2) were assessed before and after 1 week of daily subcutaneous treatment with either GH or a GH-receptor antagonist in a crossover study (EK Nr.1395/2020; Eudra-CT:2020-000831-34). The assessments comprised the quantification of IHL and hepatic ATP synthesis via magnetic resonance spectroscopy, assessment of very low-density lipoprotein (VLDL) secretion by an intralipid infusion protocol, and measurement of de novo lipogenesis (DNL) using stable isotope tracer techniques. In comparison, effects of long-term GH excess on VLDL secretion were investigated in patients with active acromegaly (54 ± 5 years; BMI 29.3 ± 3.6 kg/m2; insulin-like growth factor I of 3.1 ± 1 × upper limit of normal).
RESULTS: GH treatment stimulated the secretion of VLDL-triglycerides by 26.1% (590.5 ± 282.3 mg/h vs 738.8 ± 424.9 mg/h, P = .035). Contrarily, mean DNL doubled after GH-receptor blockage without statistical significance (3.06 ± 1.95 vs 7.32 ± 8.43%, P = .107). Effects on hepatic ATP synthesis were not observed. Baseline hepatic VLDL secretion was comparable between volunteers and patients with acromegaly.
CONCLUSION: GH modulates hepatic lipid turnover via an increase in hepatic triglyceride export and repressed GH action tends to foster DNL, which may be of assistance for the development of future therapeutic strategies against metabolic dysfunction-associated steatotic liver disease.
OBJECTIVE: This study investigated underlying antisteatotic pathways stimulated by short-term modulation of GH action.
METHODS: Ten healthy male volunteers (26 ± 5 years, body mass index [BMI] 23 ± 3.4 kg/m2) were assessed before and after 1 week of daily subcutaneous treatment with either GH or a GH-receptor antagonist in a crossover study (EK Nr.1395/2020; Eudra-CT:2020-000831-34). The assessments comprised the quantification of IHL and hepatic ATP synthesis via magnetic resonance spectroscopy, assessment of very low-density lipoprotein (VLDL) secretion by an intralipid infusion protocol, and measurement of de novo lipogenesis (DNL) using stable isotope tracer techniques. In comparison, effects of long-term GH excess on VLDL secretion were investigated in patients with active acromegaly (54 ± 5 years; BMI 29.3 ± 3.6 kg/m2; insulin-like growth factor I of 3.1 ± 1 × upper limit of normal).
RESULTS: GH treatment stimulated the secretion of VLDL-triglycerides by 26.1% (590.5 ± 282.3 mg/h vs 738.8 ± 424.9 mg/h, P = .035). Contrarily, mean DNL doubled after GH-receptor blockage without statistical significance (3.06 ± 1.95 vs 7.32 ± 8.43%, P = .107). Effects on hepatic ATP synthesis were not observed. Baseline hepatic VLDL secretion was comparable between volunteers and patients with acromegaly.
CONCLUSION: GH modulates hepatic lipid turnover via an increase in hepatic triglyceride export and repressed GH action tends to foster DNL, which may be of assistance for the development of future therapeutic strategies against metabolic dysfunction-associated steatotic liver disease.