Dataset Information

Characterization of the human preadipoyte proteome

ABSTRACT: Identification of proteome of preadipocytes isolated from morbidly obese subjects

INSTRUMENT(S): LTQ Orbitrap XL

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): White Adipose Tissue

SUBMITTER: Julia Sánchez Ceinos

LAB HEAD: María del Mar Malagón Poyato

PROVIDER: PXD015621 | Pride | 2022-02-15

REPOSITORIES: Pride

ACCESS DATA

Dataset's files

Source:

			Action	DRS
	RGR_2012_331_Fr13_121107_04.RAW	Raw
	RGR_2012_331_Fr18_121107_05.RAW	Raw
	RGR_2012_331_Fr23_121107_06.RAW	Raw
	RGR_2012_331_Fr28_33_121107_07.RAW	Raw
	RGR_2012_331_Fr3_121107_02.RAW	Raw

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Publications

Impaired mRNA splicing and proteostasis in preadipocytes in obesity-related metabolic disease.

Sánchez-Ceinos Julia J Guzmán-Ruiz Rocío R Rangel-Zúñiga Oriol Alberto OA López-Alcalá Jaime J Moreno-Caño Elena E Del Río-Moreno Mercedes M Romero-Cabrera Juan Luis JL Pérez-Martínez Pablo P Maymo-Masip Elsa E Vendrell Joan J Fernández-Veledo Sonia S Fernández-Real José Manuel JM Laurencikiene Jurga J Rydén Mikael M Membrives Antonio A Luque Raul M RM López-Miranda José J Malagón María M MM

eLife 20210921

Preadipocytes are crucial for healthy adipose tissue expansion. Preadipocyte differentiation is altered in obese individuals, which has been proposed to contribute to obesity-associated metabolic disturbances. Here, we aimed at identifying the pathogenic processes underlying impaired adipocyte differentiation in obese individuals with insulin resistance (IR)/type 2 diabetes (T2D). We report that down-regulation of a key member of the major spliceosome, <i>PRFP8</i>/PRP8, as observed in IR/T2D pr ...[more]

PMID: 34545810

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Project description:Background/aims: Serum concentrations of the hepatokine fibroblast growth factor (FGF) 21 are elevated in obesity, type‐2 diabetes, and the metabolic syndrome. We asked whether FGF21 levels differ between subjects with metabolically healthy vs. unhealthy obesity (MHO vs. MUHO) opening the possibility that FGF21 is a cross‐talker between liver and adipose tissue in MUHO. Furthermore, we studied the effects of chronic FGF21 treatment on adipocyte differentiation, lipid storage, and adipokine secretion. Methods/study design: In 20 morbidly obese donors of abdominal subcutaneous fat biopsies discordant for their whole‐body insulin sensitivity (hereby classified as MHO or MUHO subjects), serum FGF21 was quantified. The impact of chronic FGF21 treatment on differentiation, lipid accumulation, and adipokine release was assessed in isolated preadipocytes differentiated in vitro. Results: Serum FGF21 concentrations were more than two‐fold higher in MUHO as compared to 37 MHO subjects (457 ±378 vs. 211 ±123 pg/mL; p<0.05). FGF21 treatment of human preadipocytes for the entire differentiation period was modestly lipogenic (+15%; p<0.05), reduced the expression of key adipogenic transcription factors (PPARG and CEBPA, ‐15% and ‐40%, respectively; p<0.01 both), reduced adiponectin expression (‐20%; p<0.05), markedly reduced adiponectin release (‐60%; p<0.01), and substantially increased leptin (+60%; p<0.01) and interleukin‐6 (+50%; p<0.001) release. Interpretation/conclusions: The hepatokine FGF21 exerts weak lipogenic and anti‐adipogenic actions and marked adiponectin‐suppressive and leptin and interleukin‐6 release‐promoting effects in human differentiating preadipocytes. Together with the higher serum concentrations in MUHO subjects, our findings reveal FGF21 as a circulating factor promoting the development of metabolically unhealthy adipocytes. We analysed in vitro differentiated preadipocytes from 20 human donors treated with FGF21 or control cultures.