The Drosophila TNF Eiger Is an Adipokine that Acts on Insulin-Producing Cells to Mediate Nutrient Response

被引：147

作者：

Agrawal, Neha ^{[1
,3
,4
]}

Delanoue, Renald ^{[1
]}

Mauri, Alessandra ^{[1
]}

Basco, Davide ^{[2
]}

Pasco, Matthieu ^{[1
]}

Thorens, Bernard ^{[2
]}

Leopold, Pierre ^{[1
]}

机构：

[1] Univ Nice Sophia Antipolis, CNRS, INSERM, iBV, F-06100 Nice, France

[2] Univ Lausanne, Ctr Integrat Genom, CH-1015 Lausanne, Switzerland

[3] Univ Cambridge, Gurdon Inst, Tennis Court Rd, Cambridge CB2 1QN, England

[4] Univ Cambridge, Dept Physiol Dev & Neurosci, Tennis Court Rd, Cambridge CB2 1QN, England

来源：

CELL METABOLISM | 2016年 / 23卷 / 04期

基金：

欧洲研究理事会;

关键词：

NECROSIS-FACTOR-ALPHA; TYROSINE KINASE-ACTIVITY; BLOOD-BRAIN-BARRIER; ADIPOSE-TISSUE; LIFE-SPAN; OBESITY; JNK; GROWTH; RECEPTOR; RESISTANCE;

D O I：

10.1016/j.cmet.2016.03.003

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Adaptation of organisms to ever-changing nutritional environments relies on sensor tissues and systemic signals. Identification of these signals would help understand the physiological crosstalk between organs contributing to growth and metabolic homeostasis. Here we show that Eiger, the Drosophila TNF-alpha, is a metabolic hormone that mediates nutrient response by remotely acting on insulin-producing cells (IPCs). In the condition of nutrient shortage, a metalloprotease of the TNF-alpha converting enzyme (TACE) family is active in fat body (adipose-like) cells, allowing the cleavage and release of adipose Eiger in the hemolymph. In the brain IPCs, Eiger activates its receptor Grindelwald, leading to JNK-dependent inhibition of insulin production. Therefore, we have identified a humoral connexion between the fat body and the brain insulin-producing cells relying on TNF-alpha that mediates adaptive response to nutrient deprivation.

引用

页码：675 / 684

页数：10

共 56 条

[1] Suppression of Insulin Production and Secretion by a Decretin Hormone [J].