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The anti-adipogenic effect of angiotensin II on human preadipose cells involves ERK1,2 activation and PPARG
Paula Fuentes1, María José Acuña, Mariana Cifuentes
1Institute of Nutrition and Food Technology, Universidad de Chile, Casilla, Santiago, Chile.
Abstract:
Despite the importance of adipocyte formation for adipose tissue physiology, current knowledge about the mechanisms that regulate the recruitment of progenitor cells to undergo adipogenic differentiation is limited. A role for locally generated angiotensin II emerged from studies with human and murine cells. Preadipose cells from different human fat depots show reduced response to adipogenic stimuli when exposed to angiotensin II. This investigation sought to gain an insight into the intracellular mechanisms involved in the anti-adipogenic response of human preadipose cells from omental fat to angiotensin II. Its effect was evaluated on cells stimulated to adipogenic differentiation in vitro, by assessment of glycerol-3-phosphate dehydrogenase activity and expression of early markers of adipogenesis. Extracellular signal-regulated kinase(1,2) (ERK(1,2)) pathway activation was inferred from the phosphorylated to total ERK(1,2) ratio determined by western blot. Exposure to angiotensin II throughout the 10-day differentiation period resulted in a reduced adipogenic response. A similar anti-adipogenic effect was observed when this hormone was present during the first 48 h of induction to differentiation. Angiotensin II treatment had no consequences on CCAAT/enhancer-binding protein beta and peroxisome proliferator-activated receptor gamma (PPARG) induction, but increased the phosphorylated form of the key adipogenic regulator PPARG. Upon angiotensin II exposure, a raise of phosphorylated ERK(1,2) was determined, which was more prominent 8-20 h after induction of adipogenesis (when controls reached negligible values). Chemical inhibition of ERK(1,2) phosphorylation prevented angiotensin II-dependent reduction in adipogenesis. These results support the participation of the mitogen-activated protein kinase/ERK(1,2) pathway in the anti-adipogenic effect of angiotensin II on preadipose cells from human omental adipose tissue.
Insights
Angiotensin II inhibits human fat cell formation by activating the ERK1/2 pathway. This finding reveals a key mechanism in adipose tissue regulation and potential targets for metabolic disease therapies.
Area of Science:
- Cell Biology
- Endocrinology
- Metabolic Research
Background:
- Adipocyte formation is crucial for adipose tissue function, but regulatory mechanisms are not fully understood.
- Locally produced angiotensin II has been implicated in modulating adipogenesis.
- Human preadipose cells from various fat depots show reduced adipogenic potential when exposed to angiotensin II.
Purpose of the Study:
- To investigate the intracellular mechanisms underlying the anti-adipogenic effect of angiotensin II on human omental preadipose cells.
- To elucidate the role of the Extracellular Signal-Regulated Kinase (ERK) pathway in angiotensin II-mediated inhibition of adipogenesis.
Main Methods:
- Human omental preadipose cells were differentiated in vitro with and without angiotensin II exposure.
- Adipogenic differentiation was assessed by glycerol-3-phosphate dehydrogenase activity and adipogenesis marker expression.
- ERK (1,2) pathway activation was measured by Western blot analysis of phosphorylated ERK (1,2) levels.
Main Results:
- Angiotensin II significantly reduced adipogenic differentiation, an effect observed when present throughout differentiation or during the initial 48 hours.
- Angiotensin II increased phosphorylation of the adipogenic regulator PPARG and activated the ERK (1,2) pathway, particularly between 8-20 hours post-induction.
- Inhibition of ERK (1,2) phosphorylation abolished the anti-adipogenic effect of angiotensin II.
Conclusions:
- The mitogen-activated protein kinase/ERK (1,2) pathway mediates the anti-adipogenic effect of angiotensin II in human omental preadipose cells.
- These findings provide insights into the molecular mechanisms controlling fat cell formation and the role of angiotensin II in adipose tissue physiology.
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