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Updated: Nov 14, 2025

Body Composition and Metabolic Caging Analysis in High Fat Fed Mice

Body Composition and Metabolic Caging Analysis in High Fat Fed Mice

Published on: May 24, 2018

Mice lacking PC1/3 expression in POMC-expressing cells do not develop obesity.

Manita Shakya¹, Surbhi Gahlot², Anne White³

¹Department of Anatomy and Neurobiology, University of Maryland-Baltimore, Baltimore, MD.

|March 11, 2021

Summary

This summary is machine-generated.

Pro-opiomelanocortin (POMC) processing by PC1/3 enzyme is crucial for regulating body weight. Loss of PC1/3 in POMC neurons does not cause obesity, suggesting other factors are involved in PCSK1 deficiency-related weight gain.

Keywords:

Pro-opiomelanocortin obesity peptide hormone proprotein convertase 1/3 proteolysis α-MSH

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Isolation and Differentiation of Primary White and Brown Preadipocytes from Newborn Mice

Isolation and Differentiation of Primary White and Brown Preadipocytes from Newborn Mice

Published on: January 25, 2021

Area of Science:

Neuroendocrinology
Metabolic Regulation
Obesity Research

Background:

The central melanocortin system, involving pro-opiomelanocortin (POMC) neurons, regulates food intake and energy balance.
Defects in POMC processing by enzymes like prohormone convertase 1/3 (PC1/3) are linked to obesity.
The precise role of PC1/3-mediated POMC processing in body weight regulation remains unclear.

Purpose of the Study:

To investigate whether PC1/3-mediated POMC processing is essential for body weight regulation.
To determine the impact of specific, temporal knockout of Pcsk1 (gene encoding PC1/3) in POMC neurons on POMC processing and body weight.

Main Methods:

Generated a Pomc-CreER T2; Pcsk1 lox/lox mouse model for inducible knockout of Pcsk1 in POMC neurons.
Administered tamoxifen to adult mice to induce Pcsk1 deletion.
Assessed POMC cleavage into ACTH and α-MSH in the pituitary and hypothalamus.
Measured intact POMC levels and body weight in knockout and control mice.

Main Results:

Pcsk1 deletion in POMC neurons significantly impacted POMC cleavage in the pituitary but not in the hypothalamus.
Intact POMC levels were substantially elevated in mice lacking Pcsk1 in POMC neurons.
Male mice exhibited higher pituitary PC1/3 protein levels and POMC cleavage than females.
Loss of Pcsk1 solely in POMC-expressing cells did not lead to obesity.

Conclusions:

PC1/3-mediated POMC processing in POMC-expressing cells is not solely responsible for body weight regulation.
These findings challenge the hypothesis that altered POMC processing is the primary cause of obesity in cases of PCSK1 deficiency.
Obesity pathways are not disrupted by PC1/3 loss exclusively within POMC neurons.