November 2019
Volume 60Issue 11p1805-1980
Open Access
COVER: The breakdown of lipid stores from adipocytes is a critical function in adaptive
responses and communicates the status of energy stores with the rest of the homeostatic
systems of the body. During this process, known as lipolysis, adipocytes release a
newly discovered hormone called fatty acid binding protein 4, FABP4, which signals
to distant organs such as the liver and pancreas to coordinate appropriate systemic
metabolic responses and maintains glucose homeostasis. Under conditions of immunometabolic
stress and uncontrolled lipolysis, such as is the case in obesity, the circulating
levels of this counterregulatory hormone increases in an inappropriate manner and
chronically engages the otherwise adaptive short-term responses to disrupt glucose
homeostasis and set the stage for metabolic diseases such diabetes, cardiovascular
and airway diseases, and cancer. Targeting of FABP4 therefore presents a powerful
opportunity to revert the endocrine axis controlled by this hormone to a homeostatic
state to prevent and treat chronic immunometabolic diseases. (See Prentice et al. in the JLR April issue p. 734.)...Show more
COVER: The breakdown of lipid stores from adipocytes is a critical function in adaptive
responses and communicates the status of energy stores with the rest of the homeostatic
systems of the body. During this process, known as lipolysis, adipocytes release a
newly discovered hormone called fatty acid binding protein 4, FABP4, which signals
to distant organs such as the liver and pancreas to coordinate appropriate systemic
metabolic responses and maintains glucose homeostasis. Under conditions of immunometabolic
stress and uncontrolled lipolysis, such as is the case in obesity, the circulating
levels of this counterregulatory hormone increases in an inappropriate manner and
chronically engages the otherwise adaptive short-term responses to disrupt glucose
homeostasis and set the stage for metabolic diseases such diabetes, cardiovascular
and airway diseases, and cancer. Targeting of FABP4 therefore presents a powerful
opportunity to revert the endocrine axis controlled by this hormone to a homeostatic
state to prevent and treat chronic immunometabolic diseases. (See Prentice et al. in the JLR April issue p. 734.)
