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

Harvard

Magkos, F, Fabbrini, E, Mohammed, BS, Patterson, BW & Klein, S 2010, 'Increased whole-body adiposity without a concomitant increase in liver fat is not associated with augmented metabolic dysfunction', Obesity, vol. 18, no. 8, pp. 1510-1515. https://doi.org/10.1038/oby.2010.90

APA

Magkos, F., Fabbrini, E., Mohammed, B. S., Patterson, B. W., & Klein, S. (2010). Increased whole-body adiposity without a concomitant increase in liver fat is not associated with augmented metabolic dysfunction. Obesity, 18(8), 1510-1515. https://doi.org/10.1038/oby.2010.90

Vancouver

Magkos F, Fabbrini E, Mohammed BS, Patterson BW, Klein S. Increased whole-body adiposity without a concomitant increase in liver fat is not associated with augmented metabolic dysfunction. Obesity. 2010;18(8):1510-1515. https://doi.org/10.1038/oby.2010.90

Author

Magkos, Faidon ; Fabbrini, Elisa ; Mohammed, B Selma ; Patterson, Bruce W ; Klein, Samuel. / Increased whole-body adiposity without a concomitant increase in liver fat is not associated with augmented metabolic dysfunction. In: Obesity. 2010 ; Vol. 18, No. 8. pp. 1510-1515.

Bibtex

@article{bc998e793ee845829a0467ecfe36e58d,
title = "Increased whole-body adiposity without a concomitant increase in liver fat is not associated with augmented metabolic dysfunction",
abstract = "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.",
keywords = "Adult, Apolipoprotein B-100/blood, Blood Glucose/metabolism, Cholesterol, VLDL/blood, Female, Humans, Insulin/metabolism, Insulin Resistance, Lipid Metabolism, Liver/metabolism, Male, Middle Aged, Models, Theoretical, Obesity/metabolism, Palmitates/blood, Triglycerides/metabolism",
author = "Faidon Magkos and Elisa Fabbrini and Mohammed, {B Selma} and Patterson, {Bruce W} and Samuel Klein",
note = "(Ekstern)",
year = "2010",
doi = "10.1038/oby.2010.90",
language = "English",
volume = "18",
pages = "1510--1515",
journal = "Obesity",
issn = "1930-7381",
publisher = "Wiley-Blackwell",
number = "8",

}

RIS

TY - JOUR

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