Effects of Nesfatin-1 on Food Intake and Hyperglycemia

Abstract

Nesfatin-1 is a peptide derived from nucleobindin-2 and involved in the regulation of food intake and hyperglycemia. Nesfatin-1 is a recently described anorexigenic peptide, which may be involved in weight loss, malnutrition, and the regulation of appetite. Nesfatin-1 has an effect on the regulation of glucose homeostasis as well as that of food intake. The aim of this article is to bring a different perspective to the readers on the effects of nesfatin-1 on food intake and hyperglycemia. The central injection of nesfatin-1 may produce anorexigenic effects. The circulating level of nesfatin-1 is thought to be regulated by nutritional status. Long-term changes in body weight can affect nesfatin-1 levels. In overweight and obese individuals, nesfatin-1 levels may increase. Nesfatin-1 is synthesized in the hypothalamic appetite control regions. Nesfatin-1 levels may decrease in individuals with diabetes but may increase in those with impaired glucose tolerance. Nesfatin-1 may have a reducing effect on glucose levels. In addition, an increase in glucose levels may lead to an increase in the release of nesfatin-1 from pancreatic cells. Injection of nesfatin-1 can prevent hepatic glucose formation and stimulate glucose uptake. Reduction of hypothalamic nesfatin-1 levels increases hepatic glucose flow and decreases glucose uptake from peripheral tissues. In the light of all this information, nesfatin-1 may be considered to be an important regulator in the metabolic process. Nesfatin-1 appears to be able to contribute to the treatment of obesity and diabetes because of its anorexigenic and antihyperglycemic effects.

Key teaching points

• Nesfatin-1 is a anorexigenic peptide.

• Nesfatin-1 is derived from Nucleobindin-2.

• Nucleobindin-2 mRNA is produced in different areas of the brain.

• Nesfatin-1 is an inhibitory factor on appetite and a regulator of energy balance that reduces the increase in body weight.

Keywords:

• Nesfatin-1
• food intake
• hyperglycemia
• anorexigenic peptide
• obesity

Acknowledgements

No support was received from any person or institution in the process of writing this article. There are no funding and sponsorship that support the writing of the article.

Disclosure statement

There are no conflicts of interest related to this article.