Title

De Novo Lipogenesis as a Source of Second Messengers in Adipocytes

UMMS Affiliation

Program in Molecular Medicine; Graduate School of Biomedical Sciences

Publication Date

2019-11-20

Document Type

Article

Disciplines

Biochemical Phenomena, Metabolism, and Nutrition | Cellular and Molecular Physiology | Endocrine System Diseases | Endocrinology | Hormones, Hormone Substitutes, and Hormone Antagonists | Lipids | Nutritional and Metabolic Diseases | Physiological Processes

Abstract

PURPOSE OF REVIEW: Obesity is a major risk factor for type 2 diabetes. Although adipose tissue allows storage of excess calories in periods of overnutrition, in obesity, adipose tissue metabolism becomes dysregulated and can promote metabolic diseases. This review discusses recent advances in understandings how adipocyte metabolism impacts metabolic homeostasis.

RECENT FINDINGS: The ability of adipocytes to synthesize lipids from glucose is a marker of metabolic fitness, e.g., low de novo lipogenesis (DNL) in adipocytes correlates with insulin resistance in obesity. Adipocyte DNL may promote synthesis of special "insulin sensitizing" signaling lipids that act hormonally. However, each metabolic intermediate in the DNL pathway (i.e., citrate, acetyl-CoA, malonyl-CoA, and palmitate) also has second messenger functions. Mounting evidence suggests these signaling functions may also be important for maintaining healthy adipocytes. While adipocyte DNL contributes to lipid storage, lipid precursors may have additional second messenger functions critical for maintaining adipocyte health, and thus systemic metabolic homeostasis.

Keywords

Acetyl-CoA, Citrate, Insulin resistance, Malonyl-CoA, Obesity, Palmitate

DOI of Published Version

10.1007/s11892-019-1264-9

Source

Hsiao WY, Guertin DA. De Novo Lipogenesis as a Source of Second Messengers in Adipocytes. Curr Diab Rep. 2019 Nov 20;19(11):138. doi: 10.1007/s11892-019-1264-9. PMID: 31749022. Link to article on publisher's site

Journal/Book/Conference Title

Current diabetes reports

Related Resources

Link to Article in PubMed

PubMed ID

31749022

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