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脂联素和胰岛素对健康对照组和多囊卵巢综合征患者循环 CTRP-2/CTRP-9 和 GDF-8/GDF-15 的调节作用:慢性运动训练后的变化。

Regulation of circulating CTRP-2/CTRP-9 and GDF-8/GDF-15 by intralipids and insulin in healthy control and polycystic ovary syndrome women following chronic exercise training.

机构信息

Qatar Metabolic Institute, Department of Medicine and Academic Health System, Hamad Medical Corporation, Doha, Qatar.

Interim Translational Research Institute, Academic Health System, Hamad Medical Corporation, Doha, Qatar.

出版信息

Lipids Health Dis. 2021 Apr 19;20(1):34. doi: 10.1186/s12944-021-01463-3.

DOI:10.1186/s12944-021-01463-3
PMID:33874963
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8054421/
Abstract

BACKGROUND

Polycystic ovary syndrome (PCOS) is associated with obesity, diabetes, and insulin resistance. The circulating C1Q/TNF-related proteins (CTRP-2, CTRP-9) and growth differentiation factors (GDF-8, GDF-15) contribute to glucose and lipid homeostasis. The effects of intralipids and insulin infusion on CTRP-2, CTRP-9, GDF-8 and GDF-15 in PCOS and control subjects before and after chronic exercise training were examined.

METHODS

Ten PCOS and nine healthy subjects were studied at baseline status and after moderate-intensity chronic exercise training (1 h exercise, 3 times per week, 8 weeks). All participants were infused with 1.5 mL/min of saline or intralipids (20%) for 5 h, and during the last 2 h of saline or intralipids infusion hyperinsulinemic-euglycemic clamp (HIEC) was performed. CTRP-2, CTRP-9, GDF-8 and GDF-15 levels were measured at 0, 3 and 5 h.

RESULTS

Intralipids dramatically increased CTRP-2 levels in PCOS (P = 0.02) and control (P = 0.004) subjects, which was not affected by insulin infusion or by exercise. Intralipids alone had no effects on CTRP-9, GDF-8, or GDF-15. Insulin increased the levels of GDF-15 in control subjects (P = 0.05) during the saline study and in PCOS subjects (P = 0.04) during the intralipid infusion. Insulin suppressed CTRP9 levels during the intralipid study in both PCOS (P = 0.04) and control (P = 0.01) subjects. Exercise significantly reduced fasting GDF-8 levels in PCOS (P = 0.03) and control (P = 0.04) subjects; however, intralipids infusion after chronic exercise training increased GDF-8 levels in both PCOS (P = 0.003) and control (P = 0.05) subjects and insulin infusion during intralipid infusion reduced the rise of GDF-8 levels.

CONCLUSION

This study showed that exogenous lipids modulate CTRP-2, which might have a physiological role in lipid metabolism. Since chronic exercise training reduced fasting GDF-8 levels; GDF-8 might have a role in humoral adaptation to exercise. GDF-15 and CTRP-9 levels are responsive to insulin, and thus they may play a role in insulin responses.

摘要

背景

多囊卵巢综合征(PCOS)与肥胖、糖尿病和胰岛素抵抗有关。循环 C1Q/TNF 相关蛋白(CTRP-2、CTRP-9)和生长分化因子(GDF-8、GDF-15)有助于葡萄糖和脂质的动态平衡。本研究旨在探讨在慢性运动训练前后,静脉输注脂肪乳剂和胰岛素对 PCOS 患者和对照组患者的 CTRP-2、CTRP-9、GDF-8 和 GDF-15 的影响。

方法

在基线状态和中等强度慢性运动训练(1 小时运动,每周 3 次,8 周)后,研究了 10 例 PCOS 患者和 9 例健康受试者。所有参与者均以 1.5mL/min 的速度输注生理盐水或脂肪乳剂(20%)5 小时,并在最后 2 小时的生理盐水或脂肪乳剂输注期间进行高胰岛素-正常血糖钳夹(HIEC)。在 0、3 和 5 小时时测量 CTRP-2、CTRP-9、GDF-8 和 GDF-15 水平。

结果

脂肪乳剂显著增加了 PCOS(P=0.02)和对照组(P=0.004)患者的 CTRP-2 水平,而胰岛素输注或运动对此无影响。脂肪乳剂单独作用不影响 CTRP-9、GDF-8 或 GDF-15。在生理盐水研究中,胰岛素增加了对照组 GDF-15 水平(P=0.05),在脂肪乳剂输注中增加了 PCOS 患者的 GDF-15 水平(P=0.04)。在脂肪乳剂研究中,胰岛素抑制了 PCOS(P=0.04)和对照组(P=0.01)患者的 CTRP9 水平。运动显著降低了 PCOS(P=0.03)和对照组(P=0.04)患者的空腹 GDF-8 水平;然而,慢性运动训练后脂肪乳剂输注增加了 PCOS(P=0.003)和对照组(P=0.05)患者的 GDF-8 水平,而脂肪乳剂输注期间胰岛素输注降低了 GDF-8 水平的升高。

结论

本研究表明,外源性脂质调节 CTRP-2,这可能在脂质代谢中具有生理作用。由于慢性运动训练降低了空腹 GDF-8 水平,因此 GDF-8 可能在对运动的体液适应中发挥作用。GDF-15 和 CTRP-9 水平对胰岛素有反应,因此它们可能在胰岛素反应中发挥作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/552d/8054421/4276b4ccdba0/12944_2021_1463_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/552d/8054421/128736795481/12944_2021_1463_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/552d/8054421/4276b4ccdba0/12944_2021_1463_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/552d/8054421/128736795481/12944_2021_1463_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/552d/8054421/4276b4ccdba0/12944_2021_1463_Fig2_HTML.jpg

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