Insights in Nutrition and Metabolism

All submissions of the EM system will be redirected to Online Manuscript Submission System. Authors are requested to submit articles directly to Online Manuscript Submission System of respective journal.
Reach Us +1 (438) 806-1701

Opinion Article - Insights in Nutrition and Metabolism (2024) Volume 8, Issue 6

Regulation of glucose homeostasis by the central nervous system.

Angela Zerizer *

Department of Food Science, University of Foggia, Italy

*Corresponding Author:
Angela Zerizer
Department of Food Science, University of Foggia, Italy
E-mail: a.zerizer@unifg.it < /dd>

Received: 01-Nov-2024, Manuscript No. AAINM-24-151389; Editor assigned: 02-Nov-2024, PreQC No AAINM-24-151389 (PQ) Reviewed:15-Nov-2024, QC No. AAINM-24-151389 Revised:22-Nov-2024, Manuscript No. AAINM-24-151389 (R); Published:27-Nov-2024, DOI:10.35841/aainm-8.6.231

Citation: Zerizer A. Regulation of glucose homeostasis by the central nervous system. Insights Nutr Metab. 2024;8(6):231

Visit for more related articles at Insights in Nutrition and Metabolism

Introduction

Glucose homeostasis, the balance of glucose levels in the blood, is a crucial physiological process regulated by multiple organs and systems. One of the key players in maintaining this balance is the central nervous system (CNS), which integrates signals from the body to modulate glucose production, utilization, and storage. Historically, glucose regulation was primarily attributed to peripheral organs like the pancreas, liver, and muscles, but recent research highlights the central nervous system’s significant role in controlling glucose metabolism [1].

The hypothalamus, located in the brain, is central to the regulation of glucose homeostasis. It monitors blood glucose levels and responds to changes by modulating various processes that impact glucose metabolism. Specific nuclei within the hypothalamus, such as the arcuate nucleus (ARC), ventromedial nucleus (VMH), and paraventricular nucleus (PVN), play critical roles in sensing and responding to alterations in energy balance [2].

Insulin and leptin are two key hormones that communicate energy status to the CNS. Insulin, secreted by the pancreas, not only facilitates glucose uptake in peripheral tissues but also acts on the brain to regulate glucose homeostasis. Insulin receptors are present in various regions of the brain, including the hypothalamus. When insulin levels rise after a meal, insulin signaling in the hypothalamus helps suppress hepatic glucose production, contributing to the reduction of blood glucose levels [3].

Leptin, produced by adipose tissue, plays a complementary role by informing the CNS about the body’s energy reserves. Leptin receptors in the hypothalamus modulate food intake and energy expenditure. In addition to its well-known role in regulating appetite, leptin also influences glucose metabolism. Leptin signaling in the hypothalamus enhances insulin sensitivity and reduces hepatic glucose production, thereby helping to maintain stable blood glucose levels [4].

The VMH is critical for the counter-regulatory response to hypoglycemia. When blood glucose levels drop, the VMH activates the sympathetic nervous system, leading to the release of catecholamines such as epinephrine, which stimulate hepatic glucose production to restore blood glucose levels. Conversely, insulin signaling in the hypothalamus can inhibit hepatic glucose output during hyperglycemia, showcasing the dynamic regulation of glucose homeostasis by the CNS [5].

The brain has specialized mechanisms for sensing blood glucose levels, and glucose-sensing neurons are found in several brain regions, including the hypothalamus, brainstem, and cortex. These neurons respond to changes in glucose availability and adjust neuronal activity accordingly to regulate feeding behavior, insulin sensitivity, and glucose production [6].

Glucose-sensing neurons in the hypothalamus use glucose as a signaling molecule, with some neurons increasing their activity when glucose levels rise (glucose-excited neurons) and others becoming more active when glucose levels fall (glucose-inhibited neurons). This dual system allows the brain to fine-tune its responses to both hyperglycemia and hypoglycemia, ensuring glucose levels remain within a narrow range [7].

The NTS is a critical site for the regulation of the autonomic nervous system, influencing both sympathetic and parasympathetic pathways. The interaction between the brainstem and hypothalamus allows for coordinated control over both feeding behavior and glucose metabolism. For instance, activation of the parasympathetic nervous system during feeding promotes insulin secretion and glucose storage, while sympathetic activation during fasting promotes glucose mobilization [8].

The CNS also regulates glucose homeostasis through neuroendocrine pathways. The hypothalamus controls the release of hormones from the pituitary gland, which in turn affects peripheral organs involved in glucose metabolism. For example, the release of adrenocorticotropic hormone (ACTH) stimulates the adrenal glands to secrete cortisol, a hormone that increases blood glucose levels by promoting gluconeogenesis in the liver [9].

Inflammation in the brain, particularly in the hypothalamus, can disrupt glucose homeostasis. Chronic overnutrition and obesity lead to the activation of inflammatory pathways in the hypothalamus, impairing insulin and leptin signaling. This condition, known as hypothalamic inflammation, contributes to insulin resistance and the development of type 2 diabetes [10].

Conclusion

The central nervous system plays a vital and complex role in regulating glucose homeostasis through a combination of neural, hormonal, and autonomic mechanisms. The hypothalamus acts as a key integrator of signals from the periphery, modulating glucose production, utilization, and storage to maintain energy balance. Dysregulation of CNS control over glucose metabolism contributes to metabolic diseases like diabetes, highlighting the importance of this system in maintaining overall metabolic health. As research advances, the CNS’s role in glucose regulation offers promising therapeutic targets for combating metabolic disorders.

References

  1. Mirzadeh Z, Faber CL, Schwartz MW. Central nervous system control of glucose homeostasis: a therapeutic target for type 2 diabetes?. Annu Rev Pharmaco. Toxicol. 2022;62(1):55-84.

    2. Indexed at, Google Scholar, Cross Ref

  2. Lam CK, Chari M, Lam TK. CNS regulation of glucose homeostasis. Physiology. 2009;24(3):159-70.

    3. Indexed at, Google Scholar, Cross Ref

  3. Raman PG. Central nervous system control of glucose homeostasis. Open J Endocr Metab Dis. 2017;7(12):227-34.

    4. Indexed at, Google Scholar, Cross Ref

  4. Choi JH, Kim MS. Homeostatic regulation of glucose metabolism by the central nervous system. Endocrinol Metab. 2022;37(1):9-25.

    5. Indexed at, Google Scholar, Cross Ref

  5. Kumar VM. Neural regulation of glucose homeostasis. Indian J Physiol Pharmacol. 1999;43:415-24.

    6. Indexed at, Google Scholar

  6. Muntean C, Mota M, Popa S, et al. The Role of the Central Nervous System in Glucose Homeostasis. Rom J Diabetes Nutr Metab Dis. 2012;19(2):207-14.

    7. Indexed at, Google Scholar, Cross Ref

  7. Myers Jr MG, Affinati AH, Richardson N, et al. Central nervous system regulation of organismal energy and glucose homeostasis. Nat Metab. 2021;3(6):737-50.

    8. Indexed at, Google Scholar, Cross Ref

  8. Rydzewski BZ, Wozniak MM, Raizada MK. Glucose transporters in central nervous system glucose homeostasis. Molecular Biology and Physiology of Insulin and Insulin-Like Growth Factors. 1991:397-404.

    9. Indexed at, Google Scholar, Cross Ref

  9. Kleinridders A, Könner AC, Bruening JC. CNS-targets in control of energy and glucose homeostasis. Curr Opin Pharmacol. 2009;9(6):794-804.

    10. Indexed at, Google Scholar, Cross Ref

  10. Röder PV, Wu B, Liu Y, et al. Pancreatic regulation of glucose homeostasis. Exp Mol Med. 2016;48(3):e219.

    11. Indexed at, Google Scholar, Cross Ref

Get the App