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Dissecting the Brain/Islet Axis in Metabesity
Esther Fuente-Martín1, Jose M Mellado-Gil2, Nadia Cobo-Vuilleumier3
1Andalusian Center of Molecular Biology and Regenerative Medicine-CABIMER, Junta de Andalucia-University of Pablo de Olavide-University of Seville-CSIC, 41092 Seville, Spain. estherdlfuente@gmail.com.
Abstract:
The high prevalence of type 2 diabetes mellitus (T2DM), together with the fact that current treatments are only palliative and do not avoid major secondary complications, reveals the need for novel approaches to treat the cause of this disease. Efforts are currently underway to identify therapeutic targets implicated in either the regeneration or re-differentiation of a functional pancreatic islet β-cell mass to restore insulin levels and normoglycemia. However, T2DM is not only caused by failures in β-cells but also by dysfunctions in the central nervous system (CNS), especially in the hypothalamus and brainstem. Herein, we review the physiological contribution of hypothalamic neuronal and glial populations, particularly astrocytes, in the control of the systemic response that regulates blood glucose levels. The glucosensing capacity of hypothalamic astrocytes, together with their regulation by metabolic hormones, highlights the relevance of these cells in the control of glucose homeostasis. Moreover, the critical role of astrocytes in the response to inflammation, a process associated with obesity and T2DM, further emphasizes the importance of these cells as novel targets to stimulate the CNS in response to metabesity (over-nutrition-derived metabolic dysfunctions). We suggest that novel T2DM therapies should aim at stimulating the CNS astrocytic response, as well as recovering the functional pancreatic β-cell mass. Whether or not a common factor expressed in both cell types can be feasibly targeted is also discussed.
Insights
Novel type 2 diabetes mellitus (T2DM) therapies may target the central nervous system (CNS), specifically hypothalamic astrocytes, alongside pancreatic beta-cells. This approach addresses T2DM
Area of Science:
- Neuroendocrinology
- Metabolic Homeostasis
- Diabetes Pathophysiology
Background:
- Type 2 diabetes mellitus (T2DM) is prevalent, with current treatments being palliative and failing to prevent complications.
- Existing research focuses on pancreatic beta-cell regeneration, but T2DM also involves central nervous system (CNS) dysfunction.
- Hypothalamic and brainstem dysfunctions, particularly involving astrocytes, play a role in glucose regulation.
Purpose of the Study:
- To review the physiological role of hypothalamic neuronal and glial populations, especially astrocytes, in controlling systemic glucose regulation.
- To highlight astrocytes as potential therapeutic targets for T2DM and metabesity.
- To discuss the potential for targeting common factors in both CNS astrocytes and pancreatic beta-cells.
Main Methods:
- Literature review of physiological contributions of hypothalamic cells to glucose homeostasis.
- Analysis of astrocyte function in glucose sensing and metabolic hormone regulation.
- Examination of the role of astrocytes in inflammation associated with obesity and T2DM.
Main Results:
- Hypothalamic astrocytes possess glucosensing capabilities and are regulated by metabolic hormones, indicating their importance in glucose homeostasis.
- Astrocytes play a critical role in inflammatory responses linked to obesity and T2DM.
- These findings underscore the potential of targeting CNS astrocytes for T2DM treatment.
Conclusions:
- Novel T2DM therapies should consider stimulating CNS astrocytic responses in conjunction with restoring pancreatic beta-cell mass.
- Astrocytes represent a promising target for addressing metabesity-related dysfunctions.
- Investigating common therapeutic targets for both astrocytes and beta-cells warrants further research.
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