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Published on: May 4, 2021
Lumican modulates adipocyte function in obesity-associated type 2 diabetes
Clarissa Strieder-Barboza1,2,3, Carmen G Flesher1, Lynn M Geletka4
1Department of Surgery , University of Michigan Medical School, MI, USA.
Lumican, a protein linked to obesity, worsens type 2 diabetes by impairing fat cell function and insulin sensitivity. Targeting lumican may offer new treatments for diabetes-related metabolic dysfunction.
Area of Science:
- Metabolic research
- Endocrinology
- Adipose tissue biology
Background:
- Obesity and type 2 diabetes (DM) are linked to adipose tissue dysfunction.
- Lumican, a proteoglycan, is implicated in obesity, insulin resistance (IR), and adipocyte dysfunction.
Purpose of the Study:
- To investigate the role of lumican in human visceral adipose tissue (VAT) dysfunction in type 2 diabetes.
- To determine the effects of lumican on adipocyte metabolism, lipolysis, adipogenesis, and insulin sensitivity.
Main Methods:
- Analysis of lumican expression in human VAT and adipocytes from subjects with and without DM.
- Lumican knockdown experiments in adipocytes.
- Treatment of adipocytes with recombinant human lumican.
- Assessment of lipolysis, adipogenesis, and insulin sensitivity.
- Investigation of the involvement of ERK signaling pathway.
Main Results:
- Lumican expression was elevated in VAT and adipocytes of individuals with DM.
- Lumican knockdown in diabetic adipocytes improved adipogenesis and insulin sensitivity while decreasing lipolysis.
- Recombinant lumican treatment increased lipolysis and impaired insulin sensitivity in a manner dependent on ERK signaling.
Conclusions:
- Lumican impairs adipocyte metabolism in type 2 diabetes, partly through ERK signaling.
- Lumican represents a potential therapeutic target for adipose tissue-targeted treatments in DM.
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