ArticleEndocrinology, diabetes & metabolism2025
CAMKK1 in Obesity and Type 2 Diabetes Mellitus: Evidence of Interaction With Appetite-Regulating, Metabolic and Inflammatory Factors.
Article in Endocrinology, diabetes & metabolism, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Adipogenesis Under Leptin Control: Mechanisms and Model-Specific Effects.International journal of molecular sciences · 2026Review
- CAMKK1 in Obesity and Type 2 Diabetes Mellitus: Evidence of Interaction With Appetite-Regulating, Metabolic and Inflammatory Factors.Endocrinology, diabetes & metabolism · 2025Article
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Authors and funding
12 authors.
Funding
Abstract
introductionCalcium/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.
methodsCAMKK1 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.
resultsCAMKK1 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).
conclusionThese 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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