餐后脂肪酸结合蛋白 4 与肌肉胰岛素抵抗有关。

IF 8.4 1区 医学 Q1 ENDOCRINOLOGY & METABOLISM Diabetologia Pub Date : 2024-10-01 Epub Date: 2024-07-26 DOI:10.1007/s00125-024-06222-4
Tsuyoshi Okura, Yuichi Ito, Mari Anno, Satomi Endo, Sonoko Kitao, Risa Nakamura, Kazuhisa Matsumoto, Kyoko Shoji, Hiroko Okura, Kazuhiko Matsuzawa, Shoichiro Izawa, Yoshinori Ichihara, Etsuko Ueta, Masahiko Kato, Takeshi Imamura, Shin-Ichi Taniguchi, Kazuhiro Yamamoto
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引用次数: 0

摘要

目的/假设:据报道,脂肪酸结合蛋白4(FABP4)是一种肝脏胰岛素抵抗因子。我们以前曾报道,空腹 FABP4 与葡萄糖钳夹得出的胰岛素抵抗测量值相关,另一项研究报道,健康志愿者的餐后 FABP4 水平降低,但 2 型糖尿病患者的餐后 FABP4 水平未见报道(或未知)。我们对 FABP4 对肌肉细胞的直接影响了解有限。我们研究了 2 型糖尿病患者餐后 FABP4 的水平,以及肌肉胰岛素抵抗和 FABP4 的基本机制:方法:我们对 22 名 2 型糖尿病患者和 26 名非糖尿病患者进行了耐餐试验和高胰岛素血症-高血糖钳夹试验。我们测量了空腹和餐后血清 FABP4。我们培养了小鼠 C2C12 肌肉细胞,并研究了 FABP4 对葡萄糖摄取的影响。我们通过 Western 印迹和胰岛素结合试验分析了胰岛素信号:结果:2 型糖尿病患者餐后 FABP4 水平高于非糖尿病患者。除一名参与者外,无糖尿病参与者餐后 FABP4 水平低于空腹水平,而三分之一的 2 型糖尿病参与者餐后 FABP4 水平高于空腹水平。非糖尿病参与者餐后 FABP4 与葡萄糖钳夹得出的肌肉胰岛素抵抗 M/I 值相关(r=-0.42,p 结论/解释:这些结果表明,餐后 FABP4 水平与胰岛素抵抗有关,FABP4 可能会抑制胰岛素信号。
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Postprandial fatty acid-binding protein 4 is associated with muscle insulin resistance.

Aims/hypothesis: Fatty acid-binding protein 4 (FABP4) has been reported to act as a hepatic insulin resistance factor. We previously reported that fasting FABP4 was correlated with insulin resistance measurements derived from the glucose clamp, and another study reported that postprandial FABP4 levels were decreased in healthy volunteers but were not reported (or known) in participants with type 2 diabetes. We have limited knowledge about the direct effect of FABP4 on muscle cells. We investigated the postprandial FABP4 levels in participants with type 2 diabetes, and the basic mechanism of muscle insulin resistance and FABP4.

Methods: We performed a meal tolerance test and hyperinsulinaemic-euglycaemic clamp in 22 participants with type 2 diabetes and 26 participants without diabetes. We measured fasting and postprandial serum FABP4. We cultured mouse C2C12 muscle cells, and investigated the effect of FABP4 on glucose uptake. We analysed insulin signalling by western blot and insulin binding assay.

Results: The postprandial FABP4 level in participants with type 2 diabetes was higher than that in participants without diabetes. Participants without diabetes had lower postprandial FABP4 than fasting except for one participant, whereas one-third of participants with type 2 diabetes had higher postprandial FABP4 than fasting. Postprandial FABP4 was correlated with the muscle insulin resistance M/I value from a glucose clamp in participants without diabetes (r=-0.42, p<0.05). The increase in FABP4 after a meal correlated with the muscle insulin resistance M/I value (r=-0.44, p<0.05) and the difference between fasting and postprandial glucagon in participants with type 2 diabetes (r=0.36, p<0.05). FABP4 alone appears to increase glucose uptake, and the combination of FABP4 and insulin decreases glucose uptake when compared with insulin alone. FABP4 inhibits insulin signalling of muscle cells through decreases in phosphorylation of insulin receptor substrate 1 and Akt. The physiological concentration of FABP4 did not inhibit insulin binding to muscle cells.

Conclusions/interpretation: These results suggested that the postprandial FABP4 level is associated with insulin resistance, and FABP4 may suppress insulin signals.

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来源期刊
Diabetologia
Diabetologia 医学-内分泌学与代谢
CiteScore
18.10
自引率
2.40%
发文量
193
审稿时长
1 months
期刊介绍: Diabetologia, the authoritative journal dedicated to diabetes research, holds high visibility through society membership, libraries, and social media. As the official journal of the European Association for the Study of Diabetes, it is ranked in the top quartile of the 2019 JCR Impact Factors in the Endocrinology & Metabolism category. The journal boasts dedicated and expert editorial teams committed to supporting authors throughout the peer review process.
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