Official websites use .gov

A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS

A lock ( 🔒 ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

Need Help

Metabolic consequences of iron deficiency

Award Number: R21HD121779
ORGANIZATION: NATIONAL INSTITUTE OF CHILD HEALTH AND HUMAN DEVELOPMENT
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)
PERIOD OF PERFORMANCE START DATE: 07/07/2026
PERIOD OF PERFORMANCE END DATE: 06/30/2028

Group Awards By:

View Award Description

Metabolic consequences of iron deficiency - ABSTRACT Iron-deficiency anemia (IDA) affects 30% of the world’s population, with the highest prevalence in children under 5 years, and is among the leading global causes of years lived with disability. IDA is often modified by the effects of chronic infection and inflammation wherein increased concentrations of hepcidin alter the distribution of iron among tissues, and impede recovery from iron deficiency (ID). We have created a model of severe IDA in mice which better mimics the consequences of ID observed in humans. Mice were fed low iron (4ppm) diet while we increased their hepcidin (using Tmprss6 antisense oligonucleotides, ASO) to negate their efficient compensation mechanisms. As expected, the mice developed severe IDA but to our surprise they also manifested dramatic resistance to age-related and diet-induced weight gain, and lost their adipose depots. This robust phenotype provides a strong foundation for probing the effect of ID on adipose metabolism. Understanding the molecular interactions of ID with adipose metabolism is highly relevant for the management of large global populations of children who have IDA and are underweight. We therefore propose to study the mechanisms by which IDA in our clinically-relevant mouse model causes resistance to age- and HFD-induced weight gain, focusing on candidate mechanisms previously implicated in resistance to diet-induced obesity. We will examine the mechanisms in three specific aims: 1. Elucidate the effects of uncompensated systemic ID on adipose metabolism 1-1: Effect on systemic energy balance and lipid metabolism 1-2: Effect on adipose cell types and their pathways (snRNAseq) 2. Define the contribution of cellular adipose ID to resistance to obesity 2-1: Quantitation of adipose cellular iron 2-2: Local reversal of adipose ID by iron administration 2-3: Adipose pathways affected by local iron administration 3. Define the contribution of high endogenous erythropoietin (EPO) to resistance to obesity 3-1: Mice with adipose-specific deficiency of EPOR (EpoRAdiponectin-KO) 3-2: Mice with inhibited RUNX1 signaling, downstream of EpoR. The proposal addresses substantive limitations of previous studies where each examined only a single pathway for the metabolic effect of IDA. While appropriate for the discovery of new pathways, prior research did not integrate the mechanisms into a coherent and clinically relevant model. We propose to analyze the contribution of each potential mechanism in a translationally relevant acquired murine IDA model. The current project will provide the framework for more detailed analysis of the key mechanism(s), suitable for an R01-type application.


Issue Date FY	Funding FY	Legal Entity Name	Legal Entity Address	Legal Entity City	Legal Entity State	Legal Entity Zip Code	Legal Entity COUNTY	Legal Entity COUNTRY	Assistance Listing	Award Code	Budget Year	Action Date	Action Type	Action Amount

Issue Date FY: 2026 ( Subtotal = $408,843 )
2026	2026	UNIVERSITY OF CALIFORNIA, LOS ANGELES	10889 WILSHIRE BLVD STE 700	LOS ANGELES	CA	90024	LOS ANGELES	USA	Child Health and Human Development Extramural Research	000	1	7/7/2026	NEW	$408,843
														Subtotal = $408,843

Grand Total All Awards = $408,843

Top

All Categories

About

Search

Reports

Data Submission

Award Information

Metabolic consequences of iron deficiency

Award Number: R21HD121779

ORGANIZATION: NATIONAL INSTITUTE OF CHILD HEALTH AND HUMAN DEVELOPMENT

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)

PERIOD OF PERFORMANCE START DATE: 07/07/2026

PERIOD OF PERFORMANCE END DATE: 06/30/2028

Federal Websites

Department of Health & Human Services

HHS Operating Divisions

HHS Staff Divisions

Download A Document Viewer