肥胖和2型糖尿病中的CAMKK1:与食欲调节、代谢和炎症因子相互作用的证据

IF 2.6 Q3 ENDOCRINOLOGY & METABOLISM
Livio Tarchi, Lorenzo Bonacchi, Andrea Di Santo, Paolo Rovero, Chiara Sassoli, Rachele Garella, Roberta Squecco, Gianluca Villa, Romina Nassini, Francesco De Logu, Valdo Ricca, Giovanni Castellini
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引用次数: 0

摘要

钙/钙调素依赖性蛋白激酶1 (CAMKK1)通过amp活化蛋白激酶(AMPK)调节能量稳态。CAMKK1与食欲和饱腹感调节有关;然而,其在肥胖或2型糖尿病(T2DM)中的作用尚不清楚。在这项横断面研究中,主要目的是确认CAMKK1是否在糖尿病患者中升高。第二个目的是研究CAMKK1的分子相关性。方法:检索并比较肥胖(n = 3061)、T2DM (n = 4910)和对照组(n = 44257)的CAMKK1血清水平(年龄、体重指数- bmi和性别校正ANCOVA)。计算Pearson相关系数和线性回归系数(年龄和bmi调整后)。对诊断组的调节效果也进行了评估。通过混合图形模型探讨了各因素之间的相互作用。结果:与肥胖和对照组相比,T2DM患者的CAMKK1升高(事后比较,经tukey校正p = 0.010和p = 0.044)。在诊断组中,CAMKK1和AMPK呈正相关(min β > 0.400, max p β 0.070, max p)。结论:这些发现为CAMKK1在肥胖和T2DM中的作用提供了新的见解。未来的研究可能会进一步探索CAMKK1与炎症途径的相互作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

CAMKK1 in Obesity and Type 2 Diabetes Mellitus: Evidence of Interaction With Appetite-Regulating, Metabolic and Inflammatory Factors

CAMKK1 in Obesity and Type 2 Diabetes Mellitus: Evidence of Interaction With Appetite-Regulating, Metabolic and Inflammatory Factors

Introduction

Calcium/calmodulin-dependent protein kinase kinase 1 (CAMKK1) regulates energy homeostasis through AMP-activated protein kinase (AMPK). CAMKK1 has been implicated in appetite and satiety regulation; however, its role in obesity or type 2 diabetes mellitus (T2DM) remains unexplored. In this cross-sectional study, the primary aim was to confirm whether CAMKK1 is elevated in individuals with diabetes. The secondary aim was to investigate CAMKK1's molecular correlates.

Methods

CAMKK1 serum levels in individuals with obesity (n = 3,061), patients with T2DM (n = 4,910) and controls (n = 44,257) were retrieved and compared (age, body mass index—BMI and sex-adjusted ANCOVA). Pearson correlation coefficients and linear regression coefficients (age and BMI-adjusted) were computed. The moderation effect of diagnostic groups was also assessed. The interaction between factors was explored by mixed graphical models.

Results

CAMKK1 was elevated in patients with T2DM, in comparison to both individuals with obesity and controls (post hoc comparison, Tukey-adjusted p = 0.010 and p = 0.044, respectively). Across diagnostic groups, positive associations were observed between CAMKK1 and AMPK (min β > 0.400, max p < 0.001) or TNFα (min > β 0.070, max p < 0.001). A positive association with leptin (β = 0.010, p = 0.002) and ghrelin (β = 0.005, p = 0.048) was observed only within controls. Multivariate multivariable models confirmed that specific interactions between factors were disrupted in patients with T2DM (p < 0.001).

Conclusion

These findings provide new insights into the role of CAMKK1 in obesity and T2DM. Future research may further explore CAMKK1's interplay with inflammatory pathways.

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来源期刊
Endocrinology, Diabetes and Metabolism
Endocrinology, Diabetes and Metabolism Medicine-Endocrinology, Diabetes and Metabolism
CiteScore
5.00
自引率
0.00%
发文量
66
审稿时长
6 weeks
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