Mobile nav

Publication

Home >> Publications >> Publication
Millership, S., N. Ninkina, I.A. Guschina, J. Norton, R. Brambilla, P.J. Oort, S.H. Adams, R.J. Dennis, P. Voshol, J.J. Rochford and V.L. Buchman. 2012. Increased lipolysis and altered lipid homeostasis protect γ-synuclein–null mutant mice from diet-induced obesity. PNAS. 109(51):20943-20948.

Number of pages: 6

DOI: 10.1073/pnas.1210022110

Type of document: Journal Article

Download full text pdf, 1 MB; opens in new window

More information on authors/freelancers connected to LBI :
Peter Voshol, PhD


Language of document: English

Title in English: Increased lipolysis and altered lipid homeostasis protect γ-synuclein–null mutant mice from diet-induced obesity

Abstract / summary in English:

Synucleins are a family of homologous proteins principally known for their involvement in neurodegeneration. γ-Synuclein is highly expressed in human white adipose tissue and increased in obesity. Here we show that γ-synuclein is nutritionally regulated in white adipose tissue whereas its loss partially protects mice from high-fat diet (HFD)–induced obesity and ameliorates some of the associated metabolic complications. Compared with HFD-fed WT mice, HFD-fed γ-synuclein–null mutant mice display increased lipolysis, lipid oxidation, and energy expenditure, and reduced adipocyte hypertrophy. Knockdown of γ-synuclein in adipocytes causes redistribution of the key lipolytic enzyme ATGL to lipid droplets and increases lipolysis. γ-Synuclein–deficient adipocytes also contain fewer SNARE complexes of a type involved in lipid droplet fusion. We hypothesize that γ-synuclein may deliver SNAP-23 to the SNARE complexes under lipogenic conditions. Via these independent but complementary roles, γ-synuclein may coordinately modulate lipid storage by influencing lipolysis and lipid droplet formation. Our data reveal γ-synuclein as a regulator of lipid handling in adipocytes, the function of which is particularly important in conditions of nutrient excess.


Keywords in English: γ-synuclein, obesity, Type 2 Diabetes, Metabolic Syndrome, Pre-diabetes
Increased lipolysis and altered lipid homeostasis protect γ-synuclein–null mutant mice from diet-induced obesity