May 26, 2020

Lack of collagen XVIII leads to lipodystrophy and perturbs hepatic glucose and lipid homeostasis

The Journal of Physiology
Tiina PetäistöT Pihlajaniemi

Abstract

Extracellular matrix is highly remodelled in obesity and associates with the development of metabolic disorders, such as insulin resistance. Previously, we have shown that the lack of specific collagen XVIII isoforms impairs adipocyte differentiation in mice. Here, we show that mice lacking the medium and long isoforms of collagen XVIII develop insulin resistance and glucose intolerance and show elevated serum triglycerides and fat accumulation in the liver. We report that collagen XVIII-deficient mice have increased heat production at low temperatures. These results reveal a new role for collagen XVIII in the regulation of glucose and lipid metabolism, and they expand the understanding of the development of metabolic disorders. Liver and adipose tissues play important roles in the regulation of systemic glucose and lipid metabolism. Extracellular matrix synthesis and remodelling are significantly altered in these tissues in obesity and type 2 diabetes. Collagen XVIII is a ubiquitous extracellular matrix component, and it occurs in three isoforms which differ in terms of molecular size, domain structure and tissue distribution. We recently showed that, in mice, the lack of collagen XVIII, and especially its medium and long isof...Continue Reading

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Mentioned in this Paper

Obesity
Lipids
Lipid Metabolism
Hepatic
Protein Isoforms
Regulation of Biological Process
Cell Differentiation Process
Adipocytes
Size
Finding

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