Research
Hormonal
PPARgamma activation via thiazolidinediones (TZDs) like rosiglitazone and pioglitazone induces a metabolically beneficial shift in lipid repartitioning from visceral and ectopic storage (liver, muscle) to subcutaneous adipose tissue.
If you are prescribed a TZD (like pioglitazone) for diabetes, understand that any weight gain is likely shifting from dangerous visceral/organ fat to safer subcutaneous fat, which is metabolically protective.
GoodSupportsHIGH confidence
TZDs stimulate adipogenesis and cause a metabolically beneficial shift in lipid repartitioning from storage in visceral to subcutaneous adipose tissue depots as well as from ectopic storage in non-AT organs (e.g., liver muscle) to AT.
Why this rating
Supported by multiple genetic mouse models and clinical observations of TZD effects, though the paper is a review.
Source
PPARgamma in Metabolism, Immunity, and Cancer: Unified and Diverse Mechanisms of Action
Miguel Hernández-Quiles et al. · Frontiers in Endocrinology · 2021
DOI 10.3389/fendo.2021.624112
narrative_reviewCited 411×
Read the paper DOI resolved against Crossref · corpus check 2026-06-10
More from this paper
- PPARgamma mutations (loss-of-function) cause familial partial lipodystrophy type 3 (FPLD3), characterized by lack of subcutaneous fat in extremities and metabolic complications like type 2 diabetes.Strong
- PPARgamma activation in immune cells (macrophages, dendritic cells, T cells) suppresses pro-inflammatory signaling pathways (NF-kB, AP-1) via transrepression, reducing the production of inflammatory cytokines like TNF-alpha, IL-1beta, and IL-6.Good
- PPARgamma activation promotes the browning of white adipose tissue (beige adipocytes) and enhances brown adipose tissue (BAT) function, leading to increased energy expenditure and thermogenesis.Good
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