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 language | English (US) |
|---|---|
| Journal | American Journal of Physiology - Regulatory Integrative and Comparative Physiology |
| Volume | 288 |
| Issue number | 6 57-6 |
| DOIs | |
| State | Published - Jun 2005 |
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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 journal › Article
}
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 -