Resistance to ketosis in moderately obese patients: influence of fatty liver.
To elucidate whether the presence of fatty liver influences ketogenesis in obesity, the metabolic and hormonal changes in basal and low-dose epinephrine (EPI)-stimulated states were studied in 12 obese patients (OB) with normal glucose tolerance, consisting of 6 without fatty liver (OBN) and 6 with fatty liver (OBF). In the basal state, the total ketone body (TKB) concentration and the TKB to free fatty acid (FFA) ratio were significantly (p < 0.01) lower in the OBF than in the OBN group, despite elevated, but comparable, FFA levels in both groups. The basal FFA level and the TKB/FFA ratio correlated with the degree of fatty liver (p < 0.05-0.01). EPI infusion resulted in accelerated lipolysis and diminished FFA-induced ketogenesis, similar to the findings of the basal data. These results suggest that fatty liver per se is related to diminished FFA-induced ketogenesis, leading to resistance to ketosis in obesity.
Inokuchi
T
T
Second Department of Internal Medicine, Toho University School of Medicine, Tokyo, Japan.
Orita
M
M
Imamura
K
K
Takao
T
T
Isogai
S
S
D020155:3-Hydroxybutyric Acid; D000328:Adult; D001786:Blood Glucose / Q000032:analysis; D004837:Epinephrine / Q000097:blood / Q000494:pharmacology; D005230:Fatty Acids, Nonesterified / Q000097:blood; D005234:Fatty Liver / Q000150:complications / Q000378:metabolism*; D005260:Female; D005934:Glucagon / Q000097:blood; D005990:Glycerol / Q000097:blood; D006801:Humans; D006885:Hydroxybutyrates / Q000097:blood; D007113:Immunity, Innate; D007328:Insulin / Q000097:blood; D007657:Ketone Bodies / Q000096:biosynthesis*; D007662:Ketosis / Q000209:etiology / Q000276:immunology*; D008297:Male; D009765:Obesity / Q000150:complications / Q000378:metabolism*; D013997:Time Factors
D001786:Blood Glucose; D005230:Fatty Acids, Nonesterified; D006885:Hydroxybutyrates; D007328:Insulin; D007657:Ketone Bodies; D005934:Glucagon; D005990:Glycerol; D020155:3-Hydroxybutyric Acid; D004837:Epinephrine