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Lead Investigator: Michelle Foster, PhD

Institution: Colorado State University, Department of Food Science and Human Nutrition

LF Funding History: 2017 Proof of Concept Award

Hypothesis: We postulate that fat dysregulation that occurs with lipedema is caused by aberrant estrogen signaling, and will interrogate this in a rodent model.

Collaborative Opportunities: We are currently working with the laboratory of Dr. Karen Herbst to characterize ratios and concentration of estrogen and adrenergic receptors in the adipose tissue of lipedema patients. We would like to take our research a step further by collaborating with clinicians to investigate the structure of fatty nodules (fibrosis) that occur with lipedema so we can progress with understanding nodule development. We would also be interested in working closely with other lymphatic rodent researchers. 

Related News:

CSU Researcher seeks to learn more about fat tissue disorded, lipedema - CSU Source 

Project: A Mouse Model of Lipedema, Lower Subcutaneous Adipose Tissue Specific Estrogen Receptor KO

Lipedema is a condition of fat dysregulation that is characterized, in part, by site-specific fat accumulation in the region of the lower body (buttocks, hips, thighs and ankles). This condition is essentially exclusive in women and manifestation occurs with feminine hormone changes associated with puberty, pregnancy and/or menopause.  Indeed, it is postulated that lipedema is an estrogen-regulated genetic disease.

Our group will examine why puberty induces lipedema. Specifically, we postulate that fat dysregulation that occurs with lipedema is caused by aberrant estrogen signaling. Under typical circumstances, estrogen interacts with our body fat to keep it healthy while preventing the increase in fat pounds. In females interrupted estrogen-signaling results in increased body fat, pro-inflammation and subsequently fat dysregulation. We postulate lipedema presents during puberty because of the inherent lack or malfunction of estrogen receptors located on fat. A rodent model will be used to test this postulate. In particular, we will examine the contribution of estrogen receptor function specifically in the lower body fat of pre and post- puberty mice. Here we propose to produce the first mouse model with fat distribution and dysregulation similar to that described in lipedema patients. This will be accomplished using the method of estrogen receptor knock-down specifically in lower body fat.

We predict that less estrogen receptors specifically on lower body fat will increase regional fat expansion and lead to pro-inflammation by interrupting immune response encased within the regional fat. This should, however, only occur in post-puberty with mature estrogen signaling.  

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