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Identification of a regulatory pathway inhibiting adipogenesis via RSPO2
Hua Dong1, Wenfei Sun1, Yang Shen2
1Institute of Food, Nutrition and Health, ETH Zurich, Schwerzenbach, Switzerland.
Nature Metabolism
|January 14, 2022
Summary
Researchers discovered that high levels of RSPO2 protein inhibit the development of new fat cells, leading to fat tissue growth and insulin resistance in mice and potentially humans.
Area of Science:
- Metabolic health
- Cellular biology
- Endocrinology
Background:
- Healthy adipose tissue expansion relies on a balance between new fat cell formation (adipogenesis) and existing fat cell growth (hypertrophy).
- Adipogenesis is crucial for healthy adipose tissue expansion, offering protection against obesity-related insulin resistance.
Purpose of the Study:
- To investigate the roles and developmental paths of various adipogenic precursor cell populations.
- To clarify the mechanisms and cellular trajectories involved in adipogenesis.
Main Methods:
- Utilized single-cell RNA sequencing on murine adipogenic precursor datasets.
- Analyzed the functional role of RSPO2 and its interaction with the Lgr4 receptor.
Main Results:
- Identified RSPO2 as a key regulator inhibiting early progenitor maturation.
- RSPO2 is secreted by CD142+ cells, acting via the Lgr4 receptor.
- Elevated RSPO2 in mice caused adipose tissue hypertrophy and insulin resistance.
- Increased RSPO2 in obese males correlated with impaired glucose homeostasis.
Conclusions:
- Uncovered a complex cellular crosstalk mechanism that suppresses adipogenesis.
- This crosstalk impairs adipose tissue homeostasis, contributing to metabolic dysfunction.
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