Adipose tissue response to insulin following injury.
Derangements of posttraumatic glucose metabolism have long been recognized, with observed changes implicating abnormal action of insulin on target tissues. Insulin is important as well in fat metabolism, and "resistance" to insulin's effects on lipid metabolism after injury has been demonstrated. Although fat-derived fuels are the body's major energy source during starvation and after injury, most studies of posttraumatic insulin "resistance" have focused on carbohydrate metabolism. This study investigated adipose tissue response to insulin in vitro in rats subjected to starvation and/or trauma. Relationships between various parameters, including adipocyte size and weight, plasma glucose, insulin, and glycerol, and basal and insulin-suppressed lipolytic rates, were also studied. Results observed include a decrease in adipocyte size and an increase in basal lipolysis in both starved and traumatized rats, with both decreased sensitivity (T greater than S) and responsiveness (S greater than T) to insulin. These results support the concept that adipocytes of injured animals retain the ability to respond to insulin but lipolytic rates at maximal suppression are still quite high as compared to fed controls. Only minor differences were observed between starved animals and those with starvation and superimposed trauma.
Rakinic
J
J
Department of Surgery, Cook County Hospital, Chicago, IL 60612.
Takimoto
G
G
Barrett
J A
JA
Lange
D A
DA
Robin
A P
AP
D000273:Adipose Tissue / Q000503:physiopathology*; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism*; D005990:Glycerol / Q000097:blood; D007328:Insulin / Q000502:physiology*; D007333:Insulin Resistance; D008066:Lipolysis; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains; D012151:Resuscitation; D013217:Starvation / Q000503:physiopathology; D014947:Wounds and Injuries / Q000503:physiopathology*
D001786:Blood Glucose; D007328:Insulin; D005990:Glycerol