New Study Uncovers Surprising Benefits of the Protein Kallistatin

Researchers have found that after weight loss, overweight and obese people have increased levels of kallistatin in their subcutaneous white adipose tissue, a protein linked to improved metabolism and potential therapeutic benefits for the obesity and type 2 diabetes. This discovery, explored through clinical and animal studies, highlights the role of Kallistatin in improving hepatic insulin sensitivity, suggesting it as a promising target for future treatments.

New research indicates that weight loss in overweight people stimulates kallistatin expression in adipose tissue, thereby improving metabolism and presenting a new target for the treatment of obesity and type 2 diabetes.

After losing weight, overweight or obese people had increased levels of the protein Kallistatin in their subcutaneous white adipose tissue, according to a recent study by DZD researchers. Additionally, kallistatin has been shown to improve metabolism, potentially paving the way for new treatments for obesity and type 2 diabetes. The findings were recently published in the journal Molecular metabolism.

An increasing number of people are developing type 2 diabetes and obesity. These are very complex and multifaceted diseases. In order to treat them sustainably, new therapeutic approaches are necessary. Clinical studies in humans have shown that significantly overweight individuals produce less kallistatin. Kallistatin is a protein that has various effects on the body.

Among other things, it helps fight inflammation and heal wounds. The role that Kallistatin plays in glucose metabolism and its potential suitability as a therapeutic target are currently being investigated by researchers at the German Diabetes Research Center (DZD), Institute for Diabetes and Disease Research Metabolism (IDM) of Helmholtz Munich at the Eberhard-Karls University of Tübingen and Department of Diabetology, Endocrinology and Nephrology of the University Hospital of Tübingen.

Kallistatin expression increases after weight loss

To this end, they measured the expression of kallistatin in subcutaneous white adipose tissue in 47 overweight or obese people before and after weight loss. The result: kallistatin expression increases after weight loss.

Effects of Kallistatin chart

Kallistatin protein expression increases after weight loss. In mice, it improves hepatic insulin sensitivity. Credit: IDM, (email protected).

Kallistatin improves hepatic insulin sensitivity

Additionally, the researchers examined the effect of the protein in an animal model. In doing so, they observed that human kallistatin improves liver function.

Insulin is a hormone that regulates the level of glucose (sugar) in the blood. It is produced by the pancreas and released into the bloodstream when blood glucose levels rise, for example after a meal. Insulin helps transport glucose from the bloodstream to cells, where it can be used as an energy source or stored for later use. Insulin also helps regulate fat and protein metabolism. In people with diabetes, their bodies do not produce enough insulin or respond properly to insulin, leading to high blood sugar levels, which can lead to serious health problems if left untreated.

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“Our results suggest that kallistatin may be an interesting, but difficult, therapeutic target for people with obesity and insulin resistance,” says lead study author Leontine Sandforth. “Since kallistatin has insulin-sensitizing effects on the liver, it should be investigated as a potential liver-specific target to emulate the beneficial effects of weight loss and potentially treat type 2 diabetes and obesity “, adds the last author, Professor Andreas Birkenfeld.

Reference: “Role of human kallistatin in glucose and energy homeostasis in mice” by Leontine Sandforth, Sebastian Brachs, Julia Reinke, Diana Willmes, Gencer Sancar, Judith Seigner, David Juarez-Lopez, Arvid Sandforth, Jeffrey D. McBride, Jian-Xing Ma, Sven Haufe, Jens Jordan and Andreas L. Birkenfeld, February 29, 2024, Molecular metabolism.
DOI: 10.1016/j.molmet.2024.101905

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