Journal article
N. Mitkin, Vsevolod V. Pavshintcev, I. Sukhanova, I. Doronin, G. Babkin, M. Sadagurski, A. Malyshev
Pharmaceutics, 2022
Pharmaceutics, 2022
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APA
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Mitkin, N., Pavshintcev, V. V., Sukhanova, I., Doronin, I., Babkin, G., Sadagurski, M., & Malyshev, A. (2022). The Novel Peptide Chm-273s Has Therapeutic Potential for Metabolic Disorders: Evidence from In Vitro Studies and High-Sucrose Diet and High-Fat Diet Rodent Models. Pharmaceutics.
Chicago/Turabian
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Mitkin, N., Vsevolod V. Pavshintcev, I. Sukhanova, I. Doronin, G. Babkin, M. Sadagurski, and A. Malyshev. “The Novel Peptide Chm-273s Has Therapeutic Potential for Metabolic Disorders: Evidence from In Vitro Studies and High-Sucrose Diet and High-Fat Diet Rodent Models.” Pharmaceutics (2022).
MLA
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Mitkin, N., et al. “The Novel Peptide Chm-273s Has Therapeutic Potential for Metabolic Disorders: Evidence from In Vitro Studies and High-Sucrose Diet and High-Fat Diet Rodent Models.” Pharmaceutics, 2022.
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@article{n2022a,
title = {The Novel Peptide Chm-273s Has Therapeutic Potential for Metabolic Disorders: Evidence from In Vitro Studies and High-Sucrose Diet and High-Fat Diet Rodent Models},
year = {2022},
journal = {Pharmaceutics},
author = {Mitkin, N. and Pavshintcev, Vsevolod V. and Sukhanova, I. and Doronin, I. and Babkin, G. and Sadagurski, M. and Malyshev, A.}
}
Abstract
The aim of this study was to develop a novel peptide potentially applicable for the treatment of metabolic conditions, such as obesity and type 2 diabetes (T2D). We identified CHM-273S from the list of peptides from milk hydrolysate obtained by HPLC/MS-MS. In vitro analysis of primary murine fibroblasts indicated the potential of CHM-273S to upregulate IRS2 mRNA expression. CHM-273S showed a prominent anorexigenic effect in mice with the induction of a key mechanism of leptin signaling via STAT3 in the hypothalamus as a possible effector. In the animal model of metabolic disease, CHM-273S alleviated glucose intolerance and insulin resistance, and induced phosphorylation of Akt at Ser473 and Thr308 in the hepatocytes of high-sucrose diet-fed rats. In a murine model of T2D, CHM-273S mitigated high-fat diet-induced hyperglycemia and insulin resistance and improved low-grade inflammation by diminishing serum TNFα. Mice treated with chronic CHM-273S had a significant reduction in body weight, with a lower visceral fat pad weight and narrow adipocytes. The effects of the peptide administration were comparable to those of metformin. We show the potential of CHM-273S to alleviate diet-induced metabolic alterations in rodents, substantiating its further development as a therapeutic for obesity, T2D, and other metabolic conditions.