# Pennington/Louisiana NORC - Administrative Supplement for Protein restriction and senescence

> **NIH NIH P30** · LSU PENNINGTON BIOMEDICAL RESEARCH CTR · 2020 · $134,320

## Abstract

Abstract
Inflammation during obesity and aging contributes to impairments in adipose tissue leading to poor
metabolic health. Consequently, obesity induces an inflammatory environment within adipose tissue
that is associated with an irreversible cell cycle arrest known as cellular senescence. Likewise, this
inflammatory environment is detrimental to the generation of new adipocytes, impairing the
physiological role of white adipose tissue and damaging metabolic health. However, there is
substantial evidence that reducing dietary protein intake, without reducing caloric intake, protects
against HFD-induced obesity, improves glucose homeostasis, increases energy expenditure, and
remodels adipose tissue. Our lab recently discovered that the effects of dietary protein restriction
(DPR) require increases in the beneficial metabolic hormone Fibroblast Growth Factor 21 (FGF21), and
that FGF21 mediates improvements in metabolic health by acting directly within the brain. Importantly,
our data suggest that a key FGF21-dependent effect of protein restriction is the remodeling of white
adipose tissue, and we hypothesize that this adipose tissue remodeling is a primary mediator of the
improvements in metabolic health and lifespan. However, the specific changes that occur in adipose
tissue which contribute to the beneficial metabolic effects of protein restriction are not well defined.
Considering that obesity is associated with profound changes in adipose tissue, and that white adipose
tissue is a critical endocrine mediator of energy expenditure and insulin sensitivity, it is likely that diet
interventions such as DPR will reduce the metabolic insult cellular senescence and its markers, such as
p16INK4a and the senescence-associated secretory phenotype (SASP), in adipose tissue. The goal of
the current proposal is to determine if remodeling of adipose tissue by DPR reduces senescent cells,
therefore reducing the SASP in WAT. This pilot and feasibly grant will test the central hypothesis
that dietary protein restriction protects against the detrimental effects of senescent cells during
obesity.

## Key facts

- **NIH application ID:** 10192066
- **Project number:** 3P30DK072476-15S4
- **Recipient organization:** LSU PENNINGTON BIOMEDICAL RESEARCH CTR
- **Principal Investigator:** Eric Ravussin
- **Activity code:** P30 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $134,320
- **Award type:** 3
- **Project period:** 2005-07-01 → 2021-04-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10192066

## Citation

> US National Institutes of Health, RePORTER application 10192066, Pennington/Louisiana NORC - Administrative Supplement for Protein restriction and senescence (3P30DK072476-15S4). Retrieved via AI Analytics 2026-05-28 from https://api.ai-analytics.org/grant/nih/10192066. Licensed CC0.

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