TY - JOUR
T1 - Hormonal Control of Ketogenesis
T2 - Biochemical Considerations
AU - McGarry, J. D.
AU - Foster, D. W.
N1 - Funding Information:
Thisinvestigationwassupportedinpartby Public Health Service grant AM-18573 and by a grant from the American Diabetes Association. Dr.McGarryistherecipientofresearchcareer development award 1-K04-AM0763. 1.Williamson DH,HemsR:Metabolismand functionofketonebodies,inBartleyW,Korn-bergHL,QuayleJR(eds):Essaysin CellMetab- olism.JohnWileyandSonsLtd,1970,pp257\x=req-\ 281. 2. McGarry JD, Foster DW: Regulation of state. Metabolismand clinical21:471-489,aspects1972.oftheketotic
PY - 1977/4
Y1 - 1977/4
N2 - A two-site, bihormonal concept for the control of ketone body production is proposed. Thus, ketosis is viewed as the result of increased mobilization of free fatty acids from adipose tissue (site 1) to the liver (site 2), coupled with simultaneous enhancement of the liver's capacity to convert these substrates into acetoacetic and β-hydroxybutyric acids. The former event is believed to be triggered by a fall in plasma insulin levels while the latter is considered to be effected primarily by the concomitant glucagon excess characteristic of the ketotic state. Although the precise mechanism whereby elevation of the circulating [glucagon]:[insulin] ratio stimulates hepatic ketogenic potential is not known, activation of the carnitine acyltransferase reaction, the first step in the oxidation of fatty acids, is an essential feature. Two prerequisites for this metabolic adaptation in liver appear to be an elevation in its carnitine content and depletion of its glycogen stores. Despite present limitations the model (evolved mainly from rat studies) provides a framework for the description of various types of clinical ketosis in biochemical terms and may be useful for future studies.
AB - A two-site, bihormonal concept for the control of ketone body production is proposed. Thus, ketosis is viewed as the result of increased mobilization of free fatty acids from adipose tissue (site 1) to the liver (site 2), coupled with simultaneous enhancement of the liver's capacity to convert these substrates into acetoacetic and β-hydroxybutyric acids. The former event is believed to be triggered by a fall in plasma insulin levels while the latter is considered to be effected primarily by the concomitant glucagon excess characteristic of the ketotic state. Although the precise mechanism whereby elevation of the circulating [glucagon]:[insulin] ratio stimulates hepatic ketogenic potential is not known, activation of the carnitine acyltransferase reaction, the first step in the oxidation of fatty acids, is an essential feature. Two prerequisites for this metabolic adaptation in liver appear to be an elevation in its carnitine content and depletion of its glycogen stores. Despite present limitations the model (evolved mainly from rat studies) provides a framework for the description of various types of clinical ketosis in biochemical terms and may be useful for future studies.
UR - http://www.scopus.com/inward/record.url?scp=0017566802&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0017566802&partnerID=8YFLogxK
U2 - 10.1001/archinte.1977.03630160061013
DO - 10.1001/archinte.1977.03630160061013
M3 - Article
C2 - 403870
AN - SCOPUS:0017566802
SN - 0003-9926
VL - 137
SP - 495
EP - 501
JO - Archives of Internal Medicine
JF - Archives of Internal Medicine
IS - 4
ER -