Increased whole-body adiposity without a concomitant increase in liver fat is not associated with augmented metabolic dysfunction
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Increased whole-body adiposity without a concomitant increase in liver fat is not associated with augmented metabolic dysfunction. / Magkos, Faidon; Fabbrini, Elisa; Mohammed, B Selma; Patterson, Bruce W; Klein, Samuel.
In: Obesity, Vol. 18, No. 8, 2010, p. 1510-1515.Research output: Contribution to journal › Journal article › Research › peer-review
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T1 - Increased whole-body adiposity without a concomitant increase in liver fat is not associated with augmented metabolic dysfunction
AU - Magkos, Faidon
AU - Fabbrini, Elisa
AU - Mohammed, B Selma
AU - Patterson, Bruce W
AU - Klein, Samuel
N1 - (Ekstern)
PY - 2010
Y1 - 2010
N2 - Aim of this study was to determine whether an increase in adiposity, without a concomitant increase in intrahepatic triglyceride (IHTG) content, is associated with a deterioration in metabolic function. To this end, multiorgan insulin sensitivity, assessed by using a two-stage hyperinsulinemic-euglycemic clamp procedure in conjunction with stable isotopically labeled tracer infusion, and very low-density lipoprotein (VLDL) kinetics, assessed by using stable isotopically labeled tracer infusion and mathematical modeling, were determined in 10 subjects with class I obesity (BMI: 31.6 +/- 0.3 kg/m2; 37 +/- 2% body fat; visceral adipose tissue (VAT): 1,225 +/- 144 cm3) and 10 subjects with class III obesity (BMI: 41.5 +/- 0.5 kg/m2; 43 +/- 2% body fat; VAT: 2,121 +/- 378 cm3), matched on age, sex, and IHTG content (14 +/- 4 and 14 +/- 3%, respectively). No differences between class I and class III obese groups were detected in insulin-mediated suppression of palmitate (67 +/- 3 and 65 +/- 3%, respectively; P = 0.635) and glucose (67 +/- 3 and 73 +/- 5%, respectively; P = 0.348) rates of appearance in plasma, and the insulin-mediated increase in glucose disposal (218 +/- 18 and 193 +/- 30%, respectively; P = 0.489). In addition, no differences between class I and class III obese groups were detected in secretion rates of VLDL-triglyceride (6.5 +/- 1.0 and 6.0 +/- 1.4 micromol/l x min, respectively; P = 0.787) and VLDL-apolipoprotein B-100 (0.40 +/- 0.05 and 0.41 +/- 0.04 nmol/l x min, respectively; P = 0.866), and plasma clearance rates of VLDL-triglyceride (31 (16-59) and 29 (18-46) ml/min, respectively; P = 0.888) and VLDL-apolipoprotein B-100 (15 (11-19) and 17 (11-25) ml/min, respectively; P = 0.608). We conclude that increased adiposity without a concomitant increase in IHTG content does not cause additional abnormalities in adipose tissue, skeletal muscle, and hepatic insulin sensitivity, or VLDL metabolism.
AB - Aim of this study was to determine whether an increase in adiposity, without a concomitant increase in intrahepatic triglyceride (IHTG) content, is associated with a deterioration in metabolic function. To this end, multiorgan insulin sensitivity, assessed by using a two-stage hyperinsulinemic-euglycemic clamp procedure in conjunction with stable isotopically labeled tracer infusion, and very low-density lipoprotein (VLDL) kinetics, assessed by using stable isotopically labeled tracer infusion and mathematical modeling, were determined in 10 subjects with class I obesity (BMI: 31.6 +/- 0.3 kg/m2; 37 +/- 2% body fat; visceral adipose tissue (VAT): 1,225 +/- 144 cm3) and 10 subjects with class III obesity (BMI: 41.5 +/- 0.5 kg/m2; 43 +/- 2% body fat; VAT: 2,121 +/- 378 cm3), matched on age, sex, and IHTG content (14 +/- 4 and 14 +/- 3%, respectively). No differences between class I and class III obese groups were detected in insulin-mediated suppression of palmitate (67 +/- 3 and 65 +/- 3%, respectively; P = 0.635) and glucose (67 +/- 3 and 73 +/- 5%, respectively; P = 0.348) rates of appearance in plasma, and the insulin-mediated increase in glucose disposal (218 +/- 18 and 193 +/- 30%, respectively; P = 0.489). In addition, no differences between class I and class III obese groups were detected in secretion rates of VLDL-triglyceride (6.5 +/- 1.0 and 6.0 +/- 1.4 micromol/l x min, respectively; P = 0.787) and VLDL-apolipoprotein B-100 (0.40 +/- 0.05 and 0.41 +/- 0.04 nmol/l x min, respectively; P = 0.866), and plasma clearance rates of VLDL-triglyceride (31 (16-59) and 29 (18-46) ml/min, respectively; P = 0.888) and VLDL-apolipoprotein B-100 (15 (11-19) and 17 (11-25) ml/min, respectively; P = 0.608). We conclude that increased adiposity without a concomitant increase in IHTG content does not cause additional abnormalities in adipose tissue, skeletal muscle, and hepatic insulin sensitivity, or VLDL metabolism.
KW - Adult
KW - Apolipoprotein B-100/blood
KW - Blood Glucose/metabolism
KW - Cholesterol, VLDL/blood
KW - Female
KW - Humans
KW - Insulin/metabolism
KW - Insulin Resistance
KW - Lipid Metabolism
KW - Liver/metabolism
KW - Male
KW - Middle Aged
KW - Models, Theoretical
KW - Obesity/metabolism
KW - Palmitates/blood
KW - Triglycerides/metabolism
U2 - 10.1038/oby.2010.90
DO - 10.1038/oby.2010.90
M3 - Journal article
C2 - 20395947
VL - 18
SP - 1510
EP - 1515
JO - Obesity
JF - Obesity
SN - 1930-7381
IS - 8
ER -
ID: 290668051