Physical activity energy expenditure may mediate the relationship between plasma leptin levels and worsening insulin resistance independently of adiposity

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Standard

Physical activity energy expenditure may mediate the relationship between plasma leptin levels and worsening insulin resistance independently of adiposity. / Franks, P W; Loos, R J F; Brage, S; O'Rahilly, S; Wareham, N J; Ekelund, U.

In: Journal of applied physiology (Bethesda, Md. : 1985), Vol. 102, No. 5, 05.2007, p. 1921-6.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Franks, PW, Loos, RJF, Brage, S, O'Rahilly, S, Wareham, NJ & Ekelund, U 2007, 'Physical activity energy expenditure may mediate the relationship between plasma leptin levels and worsening insulin resistance independently of adiposity', Journal of applied physiology (Bethesda, Md. : 1985), vol. 102, no. 5, pp. 1921-6. https://doi.org/10.1152/japplphysiol.01022.2006

APA

Franks, P. W., Loos, R. J. F., Brage, S., O'Rahilly, S., Wareham, N. J., & Ekelund, U. (2007). Physical activity energy expenditure may mediate the relationship between plasma leptin levels and worsening insulin resistance independently of adiposity. Journal of applied physiology (Bethesda, Md. : 1985), 102(5), 1921-6. https://doi.org/10.1152/japplphysiol.01022.2006

Vancouver

Franks PW, Loos RJF, Brage S, O'Rahilly S, Wareham NJ, Ekelund U. Physical activity energy expenditure may mediate the relationship between plasma leptin levels and worsening insulin resistance independently of adiposity. Journal of applied physiology (Bethesda, Md. : 1985). 2007 May;102(5):1921-6. https://doi.org/10.1152/japplphysiol.01022.2006

Author

Franks, P W ; Loos, R J F ; Brage, S ; O'Rahilly, S ; Wareham, N J ; Ekelund, U. / Physical activity energy expenditure may mediate the relationship between plasma leptin levels and worsening insulin resistance independently of adiposity. In: Journal of applied physiology (Bethesda, Md. : 1985). 2007 ; Vol. 102, No. 5. pp. 1921-6.

Bibtex

@article{aa1c5395a2254107b9fdfdd1d6397f97,
title = "Physical activity energy expenditure may mediate the relationship between plasma leptin levels and worsening insulin resistance independently of adiposity",
abstract = "Leptin regulates a constellation of neuroendocrine processes that control energy homeostasis. The infusion of leptin in rodents lacking endogenous leptin promotes physical activity energy expenditure (PAEE) and improves insulin signaling, whereas hyperleptinemia is associated with physical inactivity and insulin resistance (IR). We tested whether baseline leptin levels predict changes in PAEE and IR over time, independent of obesity. We also assessed whether the relationship between leptin and change in IR is mediated by PAEE. The population consisted of 288 nondiabetic UK Caucasian adults (mean age: 49.4 yr; SD: 0.7 yr), in whom leptin, insulin, glucose, PAEE (via heart rate monitoring with individual calibration by indirect calorimetry), and anthropometric characteristics had been measured at baseline and 5 yr later. In linear regression models, baseline leptin levels inversely predicted follow-up PAEE (P = 0.033). On average, individuals with low leptin levels (below sex-specific median) increased their daily activity 35% more during the 5-yr follow-up period than those with above-median leptin levels. Baseline leptin level also predicted worsening IR (fasting, 30-min, and 2-h insulins, and homeostasis model assessment-IR; all P < 0.01). Associations were independent of potential confounders, such as adiposity, age, and sex. Including baseline PAEE as a cofactor in the leptin-insulin models reduced the strength (1-4% reduction) and significance of the associations, suggesting that PAEE mediates the leptin-insulin relationships. Hyperleptinemia predicts a relative decline in PAEE and worsening insulin resistance, possibly via shared molecular pathways.",
keywords = "Adiposity, Cohort Studies, Diabetes Mellitus, Type 2/etiology, Energy Metabolism, Female, Follow-Up Studies, Heart Rate, Humans, Insulin/blood, Insulin Resistance, Leptin/blood, Linear Models, Male, Middle Aged, Models, Biological, Motor Activity, Prospective Studies, Time Factors",
author = "Franks, {P W} and Loos, {R J F} and S Brage and S O'Rahilly and Wareham, {N J} and U Ekelund",
year = "2007",
month = may,
doi = "10.1152/japplphysiol.01022.2006",
language = "English",
volume = "102",
pages = "1921--6",
journal = "Journal of Applied Physiology",
issn = "8750-7587",
publisher = "American Physiological Society",
number = "5",

}

RIS

TY - JOUR

T1 - Physical activity energy expenditure may mediate the relationship between plasma leptin levels and worsening insulin resistance independently of adiposity

AU - Franks, P W

AU - Loos, R J F

AU - Brage, S

AU - O'Rahilly, S

AU - Wareham, N J

AU - Ekelund, U

PY - 2007/5

Y1 - 2007/5

N2 - Leptin regulates a constellation of neuroendocrine processes that control energy homeostasis. The infusion of leptin in rodents lacking endogenous leptin promotes physical activity energy expenditure (PAEE) and improves insulin signaling, whereas hyperleptinemia is associated with physical inactivity and insulin resistance (IR). We tested whether baseline leptin levels predict changes in PAEE and IR over time, independent of obesity. We also assessed whether the relationship between leptin and change in IR is mediated by PAEE. The population consisted of 288 nondiabetic UK Caucasian adults (mean age: 49.4 yr; SD: 0.7 yr), in whom leptin, insulin, glucose, PAEE (via heart rate monitoring with individual calibration by indirect calorimetry), and anthropometric characteristics had been measured at baseline and 5 yr later. In linear regression models, baseline leptin levels inversely predicted follow-up PAEE (P = 0.033). On average, individuals with low leptin levels (below sex-specific median) increased their daily activity 35% more during the 5-yr follow-up period than those with above-median leptin levels. Baseline leptin level also predicted worsening IR (fasting, 30-min, and 2-h insulins, and homeostasis model assessment-IR; all P < 0.01). Associations were independent of potential confounders, such as adiposity, age, and sex. Including baseline PAEE as a cofactor in the leptin-insulin models reduced the strength (1-4% reduction) and significance of the associations, suggesting that PAEE mediates the leptin-insulin relationships. Hyperleptinemia predicts a relative decline in PAEE and worsening insulin resistance, possibly via shared molecular pathways.

AB - Leptin regulates a constellation of neuroendocrine processes that control energy homeostasis. The infusion of leptin in rodents lacking endogenous leptin promotes physical activity energy expenditure (PAEE) and improves insulin signaling, whereas hyperleptinemia is associated with physical inactivity and insulin resistance (IR). We tested whether baseline leptin levels predict changes in PAEE and IR over time, independent of obesity. We also assessed whether the relationship between leptin and change in IR is mediated by PAEE. The population consisted of 288 nondiabetic UK Caucasian adults (mean age: 49.4 yr; SD: 0.7 yr), in whom leptin, insulin, glucose, PAEE (via heart rate monitoring with individual calibration by indirect calorimetry), and anthropometric characteristics had been measured at baseline and 5 yr later. In linear regression models, baseline leptin levels inversely predicted follow-up PAEE (P = 0.033). On average, individuals with low leptin levels (below sex-specific median) increased their daily activity 35% more during the 5-yr follow-up period than those with above-median leptin levels. Baseline leptin level also predicted worsening IR (fasting, 30-min, and 2-h insulins, and homeostasis model assessment-IR; all P < 0.01). Associations were independent of potential confounders, such as adiposity, age, and sex. Including baseline PAEE as a cofactor in the leptin-insulin models reduced the strength (1-4% reduction) and significance of the associations, suggesting that PAEE mediates the leptin-insulin relationships. Hyperleptinemia predicts a relative decline in PAEE and worsening insulin resistance, possibly via shared molecular pathways.

KW - Adiposity

KW - Cohort Studies

KW - Diabetes Mellitus, Type 2/etiology

KW - Energy Metabolism

KW - Female

KW - Follow-Up Studies

KW - Heart Rate

KW - Humans

KW - Insulin/blood

KW - Insulin Resistance

KW - Leptin/blood

KW - Linear Models

KW - Male

KW - Middle Aged

KW - Models, Biological

KW - Motor Activity

KW - Prospective Studies

KW - Time Factors

U2 - 10.1152/japplphysiol.01022.2006

DO - 10.1152/japplphysiol.01022.2006

M3 - Journal article

C2 - 17234803

VL - 102

SP - 1921

EP - 1926

JO - Journal of Applied Physiology

JF - Journal of Applied Physiology

SN - 8750-7587

IS - 5

ER -

ID: 258454634