Paracardial fat remodeling affects systemic metabolism through alcohol dehydrogenase 1

Petrosino, Jennifer M.; Longenecker, Jacob Z.; Ramkumar, Srinivasagan; Xu, Xianyao; Dorn, Lisa E.; Bratasz, Anna; Yu, Lianbo; Maurya, Santosh K.; Tolstikov, Vladimir; Bussberg, Valerie; Janssen, Paul M.L.; Periasamy, Muthu; Kiebish, Michael A.; Duester, Gregg; Lintig, Johannes von; Ziouzenkova, Ouliana; Accornero, Federica

doi:10.1172/jci141799

Cited by 13 publications

(13 citation statements)

References 77 publications

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“…Petrosino et al found that paracardial fat mass increased with aging and also after high-fat diet feeding. Further, the histology of the adipocytes shifted to a more white fat morphology with aging and a high-fat diet (specifically, the authors found larger, unilocular adipocytes under these conditions) compared with adipocytes in control paracardial fat (5).…”

Section: Paracardial Fat Massmentioning

confidence: 95%

“…Years of clinical research have focused on epicardial fat, which correlates with an increased risk of cardiovascular events (3,4). In a provocative study published in this issue of the JCI, Petrosino et al investigate the role of paracardial fat in whole-body metabolism and exercise physiology (5). Paracardial fat is relatively under-studied compared with other fat depots.…”

Section: Paracardial Fat Massmentioning

confidence: 99%

“…Petrosino et al used RNA-Seq to examine gene expression in paracardial fat compared with intra-abdominal fat. The authors reported increased mRNA levels of genes involved in vitamin A (retinol) metabolism, focusing in particular on alcohol dehydrogenase 1 (ADH1) (5). Vitamin A is thought to have an important role in obesity and diabetes, although much of the literature is contradictory as to the details (9).…”

Section: Exercise Performancementioning

confidence: 99%

“…Retinoic acid has diverse biologic effects that are largely mediated by the retinoic acid receptor (RAR) family of transcription factors. Petrosino et al showed that paracardial fat samples from older mice or mice fed a Western diet had decreased levels of ADH1 and that paracardial fat samples from humans with obesity also had decreased levels of ADH1 mRNA (5).…”

Section: Exercise Performancementioning

confidence: 99%

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Paracardial fat and vitamin A: a mechanism for regulating exercise performance

Joseph¹,

Morrow²

2021

Journal of Clinical Investigation

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Section: Paracardial Fat Massmentioning

confidence: 95%

Section: Paracardial Fat Massmentioning

confidence: 99%

Section: Exercise Performancementioning

confidence: 99%

Section: Exercise Performancementioning

confidence: 99%

See 2 more Smart Citations

Paracardial fat and vitamin A: a mechanism for regulating exercise performance

Joseph¹,

Morrow²

2021

Journal of Clinical Investigation

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“…Triglyceride content measurements were performed as described previously [ 36 ]. In brief, lipids were extracted from ∼25 mg of tissue and triturated under liquid nitrogen using a Cole–Parmer Scientific tissue pulverizer, followed by immediate resuspension in 250 μL ultrapure distilled water (Invitrogen).…”

Section: Methodsmentioning

confidence: 99%

Cardiac-derived TGF-β1 confers resistance to diet-induced obesity through the regulation of adipocyte size and function

Longenecker

Petrosino

Martens

et al. 2021

Molecular Metabolism

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Regulation of organismal homeostasis in response to nutrient availability is a vital physiological process that involves inter-organ communication. Understanding the mechanisms controlling systemic cross-talk for the maintenance of metabolic health is critical to counteract diet-induced obesity. Here, we show that cardiac-derived transforming growth factor beta 1 (TGF-β1) protects against weight gain and glucose intolerance in mice subjected to high-fat diet. Secretion of TGF-β1 by cardiomyocytes correlates with the bioavailability of this factor in circulation. TGF-β1 prevents adipose tissue inflammation independent of body mass and glucose metabolism phenotypes, indicating protection from adipocyte dysfunction-driven immune cell recruitment. TGF-β1 alters the gene expression programs in white adipocytes, favoring their fatty acid oxidation and consequently increasing their mitochondrial oxygen consumption rates. Ultimately, subcutaneous and visceral white adipose tissue from cadiac-specific TGF-β1 transgenic mice fail to undergo cellular hypertrophy, leading to reduced overall adiposity during high-fat feeding. Thus, TGF-β1 is a critical mediator of heart-fat communication for the regulation of systemic metabolism.

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