In this Physiology Shorts video, Taina Pihlajaniemi introduces her recent paper about how a lack of collagen XVIII leads to lipodystrophy and perturbs hepatic glucose and lipid homeostasis.
Find out more in the Journal of Physiology:
Lack of collagen XVIII leads to lipodystrophy and perturbs hepatic glucose and lipid homeostasis.
Tiina Petäistö David Vicente Kari A. Mäkelä Mikko A. Finnilä Ilkka Miinalainen Jarkko Koivunen Valerio Izzi Mari Aikio Sanna‐Maria Karppinen Raman Devarajan Jerome Thevenot Karl‐Heinz Herzig Ritva Heljasvaara Taina Pihlajaniemi
598 (16), pp. 3373-3393
https://physoc.onlinelibrary.wiley.com/doi/10.1113/JP279559
Transcript:
I am Taina Pihlajaniemi from the University of Oulu in Finland.
Our group works on the collagen family of extracellular proteins. For a long time, we have been interested in collagen type 18 on account of its complex nature.
A former PhD student, David Vicente, and a current one, Tiina Petäistö, found recently that lack of collagen 18 in mice subjected to a high-fat diet leads to reduced volumes of subcutaneous and intra-abdominal adipose tissue as shown in micro CT scans.
In analysis of the metabolic consequences of the observed lipodystrophy, we identified marked insulin resistance, glucose intolerance as well as accumulation of fat in the liver.
Changes in food intake and physical activity did not, however, explain why mice lacking collagen 18 were leaner than wild type mice.
This led us to study non-shivering thermogenesis, and indeed, when collagen 18 was lacking we observed increased heat production and formation of brown adipose tissue in cold exposure.
These results expand the understanding of adipogenesis and warrant analysis of collagen 18 in regulation of glucose and lipid metabolism also in human disorders.
We are very proud that our study became an Editor´s Choice and published in Volume 598, Issue 16. Please contact me by email if you have questions.
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