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A Comprehensive Overview of Clinical Perspectives on Melatonin a
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Der Pharmacia Lettre

Perspective - Der Pharmacia Lettre ( 2023) Volume 15, Issue 8

A Comprehensive Overview of Clinical Perspectives on Melatonin and Body Adiposity

Kenzo Suzuki*
 
Department of Health Chemistry, The University of Tokyo, Tokyo, Japan
 
*Corresponding Author:
Kenzo Suzuki, Department of Health Chemistry, The University of Tokyo, Tokyo, Japan, Email: kenzosuzuki@gmail.com

Received: 30-Jul-2023, Manuscript No. DPL-23-113020; Editor assigned: 03-Aug-2023, Pre QC No. DPL-23-113020 (PQ); Reviewed: 17-Aug-2023, QC No. DPL-23-113020; Revised: 24-Aug-2023, Manuscript No. DPL-23-113020 (R); Published: 31-Aug-2023 , DOI: 10.37532/dpl.2023.15.01 , Citations: Suzuki K. 2023. A Comprehensive Overview of Clinical Perspectives on Melatonin and Body Adiposity. Der Pharma Lett.15:01-02. ,
Copyright: 2023 Suzuki K. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Description

Adiposity, which refers to the accumulation of body fat, is a critical factor in the development of obesity, a global health concern associated with various chronic diseases, including diabetes, cardiovascular diseases, and certain types of cancer. Melatonin is produced by the pineal gland in response to darkness and has diverse physiological functions, including antioxidant, anti-inflammatory, and metabolic regulation properties. This overview explores the current state of research on the effects of melatonin on body adiposity, shedding light on its potential as a therapeutic target for obesity management.

Melatonin and its metabolic functions

Melatonin, often referred to as the "sleep hormone," plays a pivotal role in regulating the circadian rhythm and sleep patterns. However, emerging research has unveiled its involvement in various metabolic processes, including glucose homeostasis, lipid metabolism, and energy expenditure.

Regulation of energy metabolism: Melatonin receptors are distributed throughout the body, including in adipose tissue, which suggests a direct role in energy metabolism. Studies have shown that melatonin can influence energy expenditure by increasing Brown Adipose Tissue (BAT) activity, a type of fat tissue that burns calories to generate heat. BAT activation is associated with increased thermogenesis, making it a potential target for combating obesity.

Impact on lipid metabolism: Melatonin has been found to regulate lipid metabolism by influencing the expression of genes involved in lipogenesis and lipolysis. It can reduce the formation of new fat cells (adipogenesis) and promote the breakdown of stored fats (lipolysis), contributing to a decrease in adiposity. Furthermore, melatonin's antioxidant properties protect against oxidative stress, which can lead to lipid peroxidation and contribute to obesity-related complications.

Melatonin and appetite regulation

Appetite regulation is a crucial aspect of body weight maintenance, and melatonin appears to play a role in this process. While the mechanisms are not fully understood, melatonin has been shown to influence the secretion of various hormones involved in appetite control, including leptin and ghrelin.

Leptin regulation: Leptin is a hormone produced by adipose tissue that signals to the brain when the body has sufficient energy stores, leading to reduced appetite and increased energy expenditure. Studies suggest that melatonin may influence the production and sensitivity of leptin, potentially reducing appetite and promoting weight loss.

Ghrelin regulation: Conversely, ghrelin is a hormone that stimulates appetite. Melatonin has been found to suppress ghrelin secretion, which could lead to decreased food intake and lower body adiposity.

Melatonin and insulin sensitivity

Insulin resistance is a key factor in the development of obesity and type 2 diabetes. Melatonin has been shown to enhance insulin sensitivity, potentially reducing the risk of insulin resistance and its associated complications.

Glucose homeostasis: Melatonin can modulate glucose homeostasis by improving insulin sensitivity in peripheral tissues such as skeletal muscle and adipose tissue. This enhanced insulin sensitivity may help regulate blood sugar levels and reduce the risk of obesity-related metabolic disorders.

Mitochondrial function: Mitochondria are the energy-producing organelles within cells, and dysfunction in mitochondrial activity can contribute to obesity and metabolic disorders. Melatonin's antioxidant properties and ability to protect mitochondria may play a role in improving insulin sensitivity and overall metabolic health.

Conclusion

In conclusion, melatonin, primarily known for its role in regulating the sleep-wake cycle, shows potential in influencing body adiposity through its effects on energy metabolism, appetite regulation, sleep duration, and insulin sensitivity. While the mechanisms through which melatonin exerts its effects are still being elucidated, the existing evidence suggests that it may have a role in obesity management and the prevention of obesity-related metabolic complications. Overall, melatonin's multifaceted influence on various aspects of metabolism and its potential to improve sleep quality make it an intriguing target for future research and therapeutic interventions in the battle against obesity.

Citation: Suzuki K. 2023. A Comprehensive Overview of Clinical Perspectives on Melatonin and Body Adiposity. Der Pharma Lett.15:01-02.

Copyright: 2023 Suzuki K. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.