Mitochondria-Associated Membranes Response to Nutrient Availability and Role in Metabolic Diseases. (January 2017)

• Record Type: Journal Article
• Authors: Theurey, Pierre; Rieusset, Jennifer
• Is Part Of: Trends in endocrinology and metabolism. Volume 28:Number 1(2017)
• Page Start: 32
• Page End: 45
• Publication Date: 2017-01
• Subjects: insulin resistance -- metabolic flexibility -- mitochondria-associated membrane -- organelle communication -- protein phosphatase 2A; Endocrinology -- Periodicals; Metabolism -- Periodicals; Metabolism; 616.4
• DOI: 10.1016/j.tem.2016.09.002
• Languages: English
• ISSNs: 1043-2760

Abstract

Abstract : Metabolic diseases are associated with nutrient excess and metabolic inflexibility. Mitochondria and endoplasmic reticulum are important organelles and nutrient sensors, and their dysfunction has been extensively and independently implicated in metabolic diseases. Both organelles interact at sites known as mitochondria-associated membranes (MAMs), in order to exchange metabolites and calcium. Recent evidence indicates that MAM could be a hub of hepatic insulin signaling and nutrient sensing. In this review, we discuss the roles organelle function and communication play in the cell's adaptation to nutrient availability, in both physiology and metabolic diseases. We highlight how dynamic regulation of MAM affects mitochondria physiology and adaptation of cellular metabolism to nutrient availability, and how chronic MAM disruption participates in the metabolic inflexibility associated with metabolic disorders. Trends: Hepatic metabolic inflexibility promotes metabolic diseases. Mitochondria and endoplasmic reticulum (ER) are organelles with important roles in the maintainance of metabolic flexibility, and alterations in their function has been linked to metabolic desases. The ER and mitochondria interact at areas known as mitochondria-associated membranes (MAM). Emerging data suggest a role of MAM in the control of hepatic insulin signaling and metabolism. Interorganelle communication is a new glucose-sensing mechanism involved in the control of mitochondria dynamics and function. The ER–mitochondria miscommunication may be involved in the development of obesity and type 2 diabetes.