Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans.
Studies in animals have documented that, compared with glucose, dietary fructose induces dyslipidemia and insulin resistance. To assess the relative effects of these dietary sugars during sustained consumption in humans, overweight and obese subjects consumed glucose- or fructose-sweetened beverages providing 25% of energy requirements for 10 weeks. Although both groups exhibited similar weight gain during the intervention, visceral adipose volume was significantly increased only in subjects consuming fructose. Fasting plasma triglyceride concentrations increased by approximately 10% during 10 weeks of glucose consumption but not after fructose consumption. In contrast, hepatic de novo lipogenesis (DNL) and the 23-hour postprandial triglyceride AUC were increased specifically during fructose consumption. Similarly, markers of altered lipid metabolism and lipoprotein remodeling, including fasting apoB, LDL, small dense LDL, oxidized LDL, and postprandial concentrations of remnant-like particle-triglyceride and -cholesterol significantly increased during fructose but not glucose consumption. In addition, fasting plasma glucose and insulin levels increased and insulin sensitivity decreased in subjects consuming fructose but not in those consuming glucose. These data suggest that dietary fructose specifically increases DNL, promotes dyslipidemia, decreases insulin sensitivity, and increases visceral adiposity in overweight/obese adults.
Stanhope
Kimber L
KL
Department of Molecular Biosciences, UCD, Davis, California 95616, USA.
Schwarz
Jean Marc
JM
Keim
Nancy L
NL
Griffen
Steven C
SC
Bremer
Andrew A
AA
Graham
James L
JL
Hatcher
Bonnie
B
Cox
Chad L
CL
Dyachenko
Artem
A
Zhang
Wei
W
McGahan
John P
JP
Seibert
Anthony
A
Krauss
Ronald M
RM
Chiu
Sally
S
Schaefer
Ernst J
EJ
Ai
Masumi
M
Otokozawa
Seiko
S
Nakajima
Katsuyuki
K
Nakano
Takamitsu
T
Beysen
Carine
C
Hellerstein
Marc K
MK
Berglund
Lars
L
Havel
Peter J
PJ
D001628:Beverages; D001786:Blood Glucose / Q000378:metabolism; D001835:Body Weight / Q000502:physiology; D019422:Dietary Sucrose / Q000378:metabolism*; D004311:Double-Blind Method; D004435:Eating / Q000502:physiology; D002149:Energy Intake / Q000502:physiology; D005260:Female; D005632:Fructose / Q000378:metabolism*; D015870:Gene Expression / Q000235:genetics; D005947:Glucose / Q000378:metabolism*; D006801:Humans; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance / Q000502:physiology*; D050152:Intra-Abdominal Fat / Q000033:anatomy & histology / Q000378:metabolism*; D050356:Lipid Metabolism / Q000502:physiology; D008055:Lipids / Q000097:blood; D008074:Lipoproteins / Q000097:blood / Q000378:metabolism; D008099:Liver / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D008954:Models, Biological; D009765:Obesity / Q000378:metabolism; D050177:Overweight / Q000378:metabolism*; D012727:Sex Characteristics; D050151:Subcutaneous Fat / Q000378:metabolism; D014280:Triglycerides / Q000097:blood / Q000378:metabolism
D001786:Blood Glucose; D019422:Dietary Sucrose; D007328:Insulin; D008055:Lipids; D008074:Lipoproteins; D014280:Triglycerides; D005632:Fructose; D005947:Glucose