Research

Hormonal

Adipocyte-specific deletion of the NAD+-biosynthetic enzyme NAMPT causes multi-organ insulin resistance and adipose tissue dysfunction, which is reversed by administering the NAD+ precursor nicotinamide mononucleotide (NMN).

This research suggests that maintaining healthy NAD+ levels in fat tissue is crucial for preventing insulin resistance, even if you are not overweight. While this study used mice, it highlights that metabolic health is tissue-specific. For humans, this supports the broader interest in NAD+ precursors (like NMN) and lifestyle factors (like caloric restriction) that naturally boost adipose NAD+ levels, rather than focusing solely on weight loss.

GoodSupportsHIGH confidence
We found that adipocyte-specific Nampt knockout mice had severe insulin resistance in adipose tissue, liver, and skeletal muscle and adipose tissue dysfunction... These deleterious alterations were normalized by administering rosiglitazone or a key NAD+ intermediate, nicotinamide mononucleotide (NMN).
Kelly L. Stromsdorfer et al. · Cell Reports · 2016

Why this rating

High-quality mechanistic evidence using genetically modified mice (ANKO) and rigorous metabolic clamps, though limited to murine models.

Source

NAMPT-Mediated NAD+ Biosynthesis in Adipocytes Regulates Adipose Tissue Function and Multi-organ Insulin Sensitivity in Mice

Kelly L. Stromsdorfer et al. · Cell Reports · 2016

DOI 10.1016/j.celrep.2016.07.027

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DOI resolved against Crossref · corpus check 2026-06-10

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