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LCN2 blockade mitigating metabolic dysregulation and redefining appetite control in type 2 diabetes

Cifuentes-Mendiola Saúl Ernesto1, Sólis-Suarez Diana Laura1,2, Pérez-Martínez Isaac Obed3

  • 1Section of Osteimmunology and Oral Immunology, Laboratory of Dental Reseach. FES Iztacala, National Autonomous University of Mexico (UNAM), México, Mexico State, México.

Metabolic Brain Disease
|January 14, 2025
PubMed

Insights

Blocking lipocalin-2 (LCN2) in type 2 diabetes (T2D) mice improved metabolic health and normalized feeding patterns. This suggests LCN2 plays a key role in appetite regulation within the central nervous system.

Area of Science:

  • Endocrinology
  • Neuroscience
  • Metabolic Research

Background:

  • Lipocalin-2 (LCN2) is an osteokine involved in appetite regulation.
  • The role of LCN2 in central appetite regulation in type 2 diabetes (T2D) remains unclear.

Purpose of the Study:

  • To investigate the impact of blocking LCN2 on metabolic health and appetite regulation in the central nervous system of T2D mice.
  • To explore the effects of LCN2 signaling in brain regions controlling feeding behavior.

Main Methods:

  • Type 2 diabetes was induced in male C57BL/6 mice using streptozotocin and a high-carbohydrate diet.
  • LCN2 blockade was achieved via intraperitoneal administration of an anti-LCN2 antibody.
  • Metabolic parameters, feeding patterns, and brain LCN2/cFOS expression were analyzed.

Main Results:

  • T2D mice exhibited elevated serum LCN2 and altered feeding patterns, linked to disrupted LCN2-cFOS signaling in the brain.
  • Blocking LCN2 treatment improved metabolic parameters and restored normal feeding behavior after fasting.
  • Enhanced LCN2 signaling in the brain correlated with these improvements.

Conclusions:

  • Blocking LCN2 effectively restores metabolic health in T2D mice.
  • LCN2 signaling normalization in the brain is key to regulating food consumption patterns.
Keywords:
Feeding controlFeeding patternLipocalin 2Type two diabetes

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