Eicosapentaenoic fatty acid increases leptin secretion from primary cultured rat adipocytes: Role of glucose metabolism

Patricia Pérez-Matute, Amelia Marti, J. Alfredo Martínez, M. P. Fernández-Otero, Kimber Stanhope, Peter J Havel, María J. Moreno-Aliaga

Research output: Contribution to journalArticle

68 Citations (Scopus)

Abstract

Eicosapentaenoic acid (EPA), one of the n-3 polyunsaturated fatty acids, has been shown to stimulate leptin mRNA expression and secretion in 3T3-L1 cells. However, other studies have reported inhibitory effects of EPA on leptin expression and secretion in vivo and in vitro. To determine the direct effects of EPA on basal and insulin-stimulated leptin secretion, isolated rat adipocytes were incubated with EPA in the absence and presence of insulin. EPA (10, 100, and 200 μM) increased basal leptin gene expression and secretion (+43.8%, P < 0.05; +71.1%, P < 0.01; and +73.7%, P < 0.01, respectively). EPA also increased leptin secretion in the presence of 1.6 nM insulin; however, the effect was less pronounced than in the absence of it. Because adipocyte glucose and lipid metabolism are involved in the regulation of leptin production, the metabolic effects of this fatty acid were also examined. EPA (200 μM) increased basal glucose uptake in isolated adipocytes (+50%, P < 0.05). Anaerobic metabolism of glucose, as assessed by lactate production and proportion of glucose metabolized to lactate, has been shown to be inversely correlated to leptin secretion and was decreased by EPA in both the absence and presence of insulin. EPA increased basal glucose oxidation as determined by the proportion of 14C-labeled glucose metabolized to CO2. Lipogenesis (14C-labeled glucose incorporation into triglyceride) was decreased by EPA in the absence of insulin, whereas lipolysis (glycerol release) was unaffected. The EPA-induced increase of basal leptin secretion was highly correlated with increased glucose utilization (r = +0.89, P < 0.01) and inversely related to the anaerobic glucose metabolism to lactate. EPA's effect on insulin-stimulated leptin secretion was not related to increased glucose utilization but was inversely correlated with anaerobic glucose metabolism to lactate (r = -0.84, P < 0.01). Together, the results suggest that EPA, like insulin, stimulates leptin production by increasing the nonanaerobic/oxidative metabolism of glucose.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Volume288
Issue number6 57-6
DOIs
StatePublished - Jun 2005

Fingerprint

Eicosapentaenoic Acid
Leptin
Adipocytes
Fatty Acids
Glucose
Insulin
Anaerobiosis
Lactic Acid
3T3-L1 Cells
Lipogenesis
Lipolysis
Omega-3 Fatty Acids
Lipid Metabolism
Glycerol
Triglycerides

Keywords

  • ω-3 polyunsaturated fatty acids
  • Adipose tissue
  • Diabetes
  • Obesity

ASJC Scopus subject areas

  • Physiology

Cite this

Eicosapentaenoic fatty acid increases leptin secretion from primary cultured rat adipocytes : Role of glucose metabolism. / Pérez-Matute, Patricia; Marti, Amelia; Martínez, J. Alfredo; Fernández-Otero, M. P.; Stanhope, Kimber; Havel, Peter J; Moreno-Aliaga, María J.

In: American Journal of Physiology - Regulatory Integrative and Comparative Physiology, Vol. 288, No. 6 57-6, 06.2005.

Research output: Contribution to journalArticle

Pérez-Matute, Patricia ; Marti, Amelia ; Martínez, J. Alfredo ; Fernández-Otero, M. P. ; Stanhope, Kimber ; Havel, Peter J ; Moreno-Aliaga, María J. / Eicosapentaenoic fatty acid increases leptin secretion from primary cultured rat adipocytes : Role of glucose metabolism. In: American Journal of Physiology - Regulatory Integrative and Comparative Physiology. 2005 ; Vol. 288, No. 6 57-6.
@article{4dabe8a276b44790bbb9c1ef1110242b,
title = "Eicosapentaenoic fatty acid increases leptin secretion from primary cultured rat adipocytes: Role of glucose metabolism",
abstract = "Eicosapentaenoic acid (EPA), one of the n-3 polyunsaturated fatty acids, has been shown to stimulate leptin mRNA expression and secretion in 3T3-L1 cells. However, other studies have reported inhibitory effects of EPA on leptin expression and secretion in vivo and in vitro. To determine the direct effects of EPA on basal and insulin-stimulated leptin secretion, isolated rat adipocytes were incubated with EPA in the absence and presence of insulin. EPA (10, 100, and 200 μM) increased basal leptin gene expression and secretion (+43.8{\%}, P < 0.05; +71.1{\%}, P < 0.01; and +73.7{\%}, P < 0.01, respectively). EPA also increased leptin secretion in the presence of 1.6 nM insulin; however, the effect was less pronounced than in the absence of it. Because adipocyte glucose and lipid metabolism are involved in the regulation of leptin production, the metabolic effects of this fatty acid were also examined. EPA (200 μM) increased basal glucose uptake in isolated adipocytes (+50{\%}, P < 0.05). Anaerobic metabolism of glucose, as assessed by lactate production and proportion of glucose metabolized to lactate, has been shown to be inversely correlated to leptin secretion and was decreased by EPA in both the absence and presence of insulin. EPA increased basal glucose oxidation as determined by the proportion of 14C-labeled glucose metabolized to CO2. Lipogenesis (14C-labeled glucose incorporation into triglyceride) was decreased by EPA in the absence of insulin, whereas lipolysis (glycerol release) was unaffected. The EPA-induced increase of basal leptin secretion was highly correlated with increased glucose utilization (r = +0.89, P < 0.01) and inversely related to the anaerobic glucose metabolism to lactate. EPA's effect on insulin-stimulated leptin secretion was not related to increased glucose utilization but was inversely correlated with anaerobic glucose metabolism to lactate (r = -0.84, P < 0.01). Together, the results suggest that EPA, like insulin, stimulates leptin production by increasing the nonanaerobic/oxidative metabolism of glucose.",
keywords = "ω-3 polyunsaturated fatty acids, Adipose tissue, Diabetes, Obesity",
author = "Patricia P{\'e}rez-Matute and Amelia Marti and Mart{\'i}nez, {J. Alfredo} and Fern{\'a}ndez-Otero, {M. P.} and Kimber Stanhope and Havel, {Peter J} and Moreno-Aliaga, {Mar{\'i}a J.}",
year = "2005",
month = "6",
doi = "10.1152/ajpregu.00727.2004",
language = "English (US)",
volume = "288",
journal = "American Journal of Physiology - Renal Fluid and Electrolyte Physiology",
issn = "1931-857X",
publisher = "American Physiological Society",
number = "6 57-6",

}

TY - JOUR

T1 - Eicosapentaenoic fatty acid increases leptin secretion from primary cultured rat adipocytes

T2 - Role of glucose metabolism

AU - Pérez-Matute, Patricia

AU - Marti, Amelia

AU - Martínez, J. Alfredo

AU - Fernández-Otero, M. P.

AU - Stanhope, Kimber

AU - Havel, Peter J

AU - Moreno-Aliaga, María J.

PY - 2005/6

Y1 - 2005/6

N2 - Eicosapentaenoic acid (EPA), one of the n-3 polyunsaturated fatty acids, has been shown to stimulate leptin mRNA expression and secretion in 3T3-L1 cells. However, other studies have reported inhibitory effects of EPA on leptin expression and secretion in vivo and in vitro. To determine the direct effects of EPA on basal and insulin-stimulated leptin secretion, isolated rat adipocytes were incubated with EPA in the absence and presence of insulin. EPA (10, 100, and 200 μM) increased basal leptin gene expression and secretion (+43.8%, P < 0.05; +71.1%, P < 0.01; and +73.7%, P < 0.01, respectively). EPA also increased leptin secretion in the presence of 1.6 nM insulin; however, the effect was less pronounced than in the absence of it. Because adipocyte glucose and lipid metabolism are involved in the regulation of leptin production, the metabolic effects of this fatty acid were also examined. EPA (200 μM) increased basal glucose uptake in isolated adipocytes (+50%, P < 0.05). Anaerobic metabolism of glucose, as assessed by lactate production and proportion of glucose metabolized to lactate, has been shown to be inversely correlated to leptin secretion and was decreased by EPA in both the absence and presence of insulin. EPA increased basal glucose oxidation as determined by the proportion of 14C-labeled glucose metabolized to CO2. Lipogenesis (14C-labeled glucose incorporation into triglyceride) was decreased by EPA in the absence of insulin, whereas lipolysis (glycerol release) was unaffected. The EPA-induced increase of basal leptin secretion was highly correlated with increased glucose utilization (r = +0.89, P < 0.01) and inversely related to the anaerobic glucose metabolism to lactate. EPA's effect on insulin-stimulated leptin secretion was not related to increased glucose utilization but was inversely correlated with anaerobic glucose metabolism to lactate (r = -0.84, P < 0.01). Together, the results suggest that EPA, like insulin, stimulates leptin production by increasing the nonanaerobic/oxidative metabolism of glucose.

AB - Eicosapentaenoic acid (EPA), one of the n-3 polyunsaturated fatty acids, has been shown to stimulate leptin mRNA expression and secretion in 3T3-L1 cells. However, other studies have reported inhibitory effects of EPA on leptin expression and secretion in vivo and in vitro. To determine the direct effects of EPA on basal and insulin-stimulated leptin secretion, isolated rat adipocytes were incubated with EPA in the absence and presence of insulin. EPA (10, 100, and 200 μM) increased basal leptin gene expression and secretion (+43.8%, P < 0.05; +71.1%, P < 0.01; and +73.7%, P < 0.01, respectively). EPA also increased leptin secretion in the presence of 1.6 nM insulin; however, the effect was less pronounced than in the absence of it. Because adipocyte glucose and lipid metabolism are involved in the regulation of leptin production, the metabolic effects of this fatty acid were also examined. EPA (200 μM) increased basal glucose uptake in isolated adipocytes (+50%, P < 0.05). Anaerobic metabolism of glucose, as assessed by lactate production and proportion of glucose metabolized to lactate, has been shown to be inversely correlated to leptin secretion and was decreased by EPA in both the absence and presence of insulin. EPA increased basal glucose oxidation as determined by the proportion of 14C-labeled glucose metabolized to CO2. Lipogenesis (14C-labeled glucose incorporation into triglyceride) was decreased by EPA in the absence of insulin, whereas lipolysis (glycerol release) was unaffected. The EPA-induced increase of basal leptin secretion was highly correlated with increased glucose utilization (r = +0.89, P < 0.01) and inversely related to the anaerobic glucose metabolism to lactate. EPA's effect on insulin-stimulated leptin secretion was not related to increased glucose utilization but was inversely correlated with anaerobic glucose metabolism to lactate (r = -0.84, P < 0.01). Together, the results suggest that EPA, like insulin, stimulates leptin production by increasing the nonanaerobic/oxidative metabolism of glucose.

KW - ω-3 polyunsaturated fatty acids

KW - Adipose tissue

KW - Diabetes

KW - Obesity

UR - http://www.scopus.com/inward/record.url?scp=19344368463&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=19344368463&partnerID=8YFLogxK

U2 - 10.1152/ajpregu.00727.2004

DO - 10.1152/ajpregu.00727.2004

M3 - Article

C2 - 15650121

AN - SCOPUS:19344368463

VL - 288

JO - American Journal of Physiology - Renal Fluid and Electrolyte Physiology

JF - American Journal of Physiology - Renal Fluid and Electrolyte Physiology

SN - 1931-857X

IS - 6 57-6

ER -