# Intestinal Intelectin-1 regulation of obesity development

> **NIH NIH K08** · MASSACHUSETTS GENERAL HOSPITAL · 2024 · $26,289

## Abstract

PROJECT SUMMARY/ABSTRACT
 This proposal describes a 4-year career mentored research project with the goal of defining the effects of
intestinal Intelectin-1 (ITLN1) in microbial function and composition and its role in the genesis of obesity and
early life weight gain. Successful completion of the research and training plan will enable the investigator to gain
the skills necessary to secure independent funding and become an independent physician-scientist. The inves-
tigator's long-term goal is to define how the host-microbiota interface modulates the risk of obesity early in life
through multidisciplinary approaches and enable the design of preventative obesity strategies starting in the
neonatal period. The research aims and career development plan will work towards mastery and independence
in gnotobiology, gut anaerobic microbiology, and preclinical models of metabolism and proficiency in functional
and bioinformatic analysis of the microbiota and translational research in early life. The primary co-mentors are
Dr. Richard S. Blumberg – an expert in mucosal immunology and preclinical models to study gut-microbiota
interactions – and Dr. Alessio Fasano – a leader in pediatric translational studies in the host-microbiome interface
–at Mass General Brigham/Harvard Medical School. The collaborative and mentorship team comprises a local,
multi-institutional group of experts in bioinformatics, intestinal microbial ecology, mucosal immunology, metabo-
lism, and childhood obesity. The research proposal seeks to explore interactions between intestinal ITLN1 and
microbes in the genesis of obesity. ITLN1 has been associated with obesity in humans, but the mechanism(s)
behind(s) this association are unknown. The preliminary findings suggest that ITLN1 binds a particular subset of
bacteria in vivo and modulates the metabolic activity of the microbiome. Furthermore, intestinal ITLN1 might
protect against obesity in a microbiota-dependent manner. The overall hypothesis of this mentored research is
that intestinal ITLN1 protects from obesity by modulating the metabolic activity of ITLN1-bound bacteria. In this
proposal, we will use in vitro transcriptomic and phenotypic analysis of ITLN1-bound bacteria and bottom-up and
bottom down microbiological approaches in conventional and gnotobiotic mice with and without ITLN1 to under-
stand the effects of ITLN1 on intestinal microbes and seek to provide critical information about mechanisms by
which ITLN1 in the intestine can influence the host-susceptibility to obesity. Furthermore, the applicant will ex-
plore the translational implication of ITLN1 binding to microbes in infants with adequate and excessive weight
gain during the first two years of life, as rapid weight gain in this critical window is associated with childhood
obesity. Expected outcomes include direct evidence that loss of a single protein (ITLN1) in the intestinal epithe-
lium leads to obesity and metabolic syndrome through its effects on the micro...

## Key facts

- **NIH application ID:** 10877001
- **Project number:** 5K08DK133639-02
- **Recipient organization:** MASSACHUSETTS GENERAL HOSPITAL
- **Principal Investigator:** Juan D. Matute
- **Activity code:** K08 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2024
- **Award amount:** $26,289
- **Award type:** 5
- **Project period:** 2023-07-01 → 2024-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10877001

## Citation

> US National Institutes of Health, RePORTER application 10877001, Intestinal Intelectin-1 regulation of obesity development (5K08DK133639-02). Retrieved via AI Analytics 2026-05-24 from https://api.ai-analytics.org/grant/nih/10877001. Licensed CC0.

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