FABP4 is secreted from adipocytes by adenyl cyclase-PKA- and guanylyl cyclase-PKG-dependent lipolytic mechanisms

Tomohiro Mita, Masato Furuhashi, Shinya Hiramitsu, Junichi Ishii, Kyoko Hoshina, Shutaro Ishimura, Takahiro Fuseya, Yuki Watanabe, Marenao Tanaka, Kohei Ohno, Hiroshi Akasaka, Hirofumi Ohnishi, Hideaki Yoshida, Shigeyuki Saitoh, Kazuaki Shimamoto, Tetsuji Miura

Research output: Contribution to journalArticle

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Abstract

Objective Fatty acid-binding protein 4 (FABP4) is expressed in adipocytes, and elevated plasma FABP4 level is associated with obesity-mediated metabolic phenotype. Postprandial regulation and secretory signaling of FABP4 has been investigated. Methods Time courses of FABP4 levels were examined during an oral glucose tolerance test (OGTT; n = 53) or a high-fat test meal eating (n = 35). Effects of activators and inhibitors of adenyl cyclase (AC)-protein kinase A (PKA) signaling and guanylyl cyclase (GC)-protein kinase G (PKG) signaling on FABP4 secretion from mouse 3T3-L1 adipocytes were investigated. Results FABP4 level significantly declined after the OGTT or a high-fat meal eating, while insulin level was increased. Treatment with low and high glucose concentration or palmitate for 2 h did not affect FABP4 secretion from 3T3-L1 adipocytes. FABP4 secretion was increased by stimulation of lipolysis using isoproterenol, a β3-adrenoceptor agonist (CL316243), forskolin, dibutyryl-cAMP and atrial natriuretic peptide, and the induced FABP4 secretion was suppressed by insulin or an inhibitor of PKA (H-89), PKG (KT5823) or hormone sensitive lipase (CAY10499). Conclusions FABP4 is secreted from adipocytes in association with lipolysis regulated by AC-PKA- and GC-PKG-mediated signal pathways. Plasma FABP4 level declines postprandially, and suppression of FABP4 secretion by insulin-induced anti-lipolytic signaling may be involved in this decline in FABP4 level.

Original languageEnglish
Pages (from-to)359-367
Number of pages9
JournalObesity
Volume23
Issue number2
DOIs
Publication statusPublished - 01-02-2015

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Cyclic GMP-Dependent Protein Kinases
Fatty Acid-Binding Proteins
Guanylate Cyclase
Cyclic AMP-Dependent Protein Kinases
Adenylyl Cyclases
Adipocytes
Glucose Tolerance Test
Lipolysis
Insulin
Meals
Blood Proteins
Eating
Fats
Sterol Esterase
Palmitates
Atrial Natriuretic Factor
Colforsin
Isoproterenol
Adrenergic Receptors
Signal Transduction

All Science Journal Classification (ASJC) codes

  • Medicine (miscellaneous)
  • Endocrinology, Diabetes and Metabolism
  • Endocrinology
  • Nutrition and Dietetics

Cite this

Mita, T., Furuhashi, M., Hiramitsu, S., Ishii, J., Hoshina, K., Ishimura, S., ... Miura, T. (2015). FABP4 is secreted from adipocytes by adenyl cyclase-PKA- and guanylyl cyclase-PKG-dependent lipolytic mechanisms. Obesity, 23(2), 359-367. https://doi.org/10.1002/oby.20954
Mita, Tomohiro ; Furuhashi, Masato ; Hiramitsu, Shinya ; Ishii, Junichi ; Hoshina, Kyoko ; Ishimura, Shutaro ; Fuseya, Takahiro ; Watanabe, Yuki ; Tanaka, Marenao ; Ohno, Kohei ; Akasaka, Hiroshi ; Ohnishi, Hirofumi ; Yoshida, Hideaki ; Saitoh, Shigeyuki ; Shimamoto, Kazuaki ; Miura, Tetsuji. / FABP4 is secreted from adipocytes by adenyl cyclase-PKA- and guanylyl cyclase-PKG-dependent lipolytic mechanisms. In: Obesity. 2015 ; Vol. 23, No. 2. pp. 359-367.
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title = "FABP4 is secreted from adipocytes by adenyl cyclase-PKA- and guanylyl cyclase-PKG-dependent lipolytic mechanisms",
abstract = "Objective Fatty acid-binding protein 4 (FABP4) is expressed in adipocytes, and elevated plasma FABP4 level is associated with obesity-mediated metabolic phenotype. Postprandial regulation and secretory signaling of FABP4 has been investigated. Methods Time courses of FABP4 levels were examined during an oral glucose tolerance test (OGTT; n = 53) or a high-fat test meal eating (n = 35). Effects of activators and inhibitors of adenyl cyclase (AC)-protein kinase A (PKA) signaling and guanylyl cyclase (GC)-protein kinase G (PKG) signaling on FABP4 secretion from mouse 3T3-L1 adipocytes were investigated. Results FABP4 level significantly declined after the OGTT or a high-fat meal eating, while insulin level was increased. Treatment with low and high glucose concentration or palmitate for 2 h did not affect FABP4 secretion from 3T3-L1 adipocytes. FABP4 secretion was increased by stimulation of lipolysis using isoproterenol, a β3-adrenoceptor agonist (CL316243), forskolin, dibutyryl-cAMP and atrial natriuretic peptide, and the induced FABP4 secretion was suppressed by insulin or an inhibitor of PKA (H-89), PKG (KT5823) or hormone sensitive lipase (CAY10499). Conclusions FABP4 is secreted from adipocytes in association with lipolysis regulated by AC-PKA- and GC-PKG-mediated signal pathways. Plasma FABP4 level declines postprandially, and suppression of FABP4 secretion by insulin-induced anti-lipolytic signaling may be involved in this decline in FABP4 level.",
author = "Tomohiro Mita and Masato Furuhashi and Shinya Hiramitsu and Junichi Ishii and Kyoko Hoshina and Shutaro Ishimura and Takahiro Fuseya and Yuki Watanabe and Marenao Tanaka and Kohei Ohno and Hiroshi Akasaka and Hirofumi Ohnishi and Hideaki Yoshida and Shigeyuki Saitoh and Kazuaki Shimamoto and Tetsuji Miura",
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Mita, T, Furuhashi, M, Hiramitsu, S, Ishii, J, Hoshina, K, Ishimura, S, Fuseya, T, Watanabe, Y, Tanaka, M, Ohno, K, Akasaka, H, Ohnishi, H, Yoshida, H, Saitoh, S, Shimamoto, K & Miura, T 2015, 'FABP4 is secreted from adipocytes by adenyl cyclase-PKA- and guanylyl cyclase-PKG-dependent lipolytic mechanisms', Obesity, vol. 23, no. 2, pp. 359-367. https://doi.org/10.1002/oby.20954

FABP4 is secreted from adipocytes by adenyl cyclase-PKA- and guanylyl cyclase-PKG-dependent lipolytic mechanisms. / Mita, Tomohiro; Furuhashi, Masato; Hiramitsu, Shinya; Ishii, Junichi; Hoshina, Kyoko; Ishimura, Shutaro; Fuseya, Takahiro; Watanabe, Yuki; Tanaka, Marenao; Ohno, Kohei; Akasaka, Hiroshi; Ohnishi, Hirofumi; Yoshida, Hideaki; Saitoh, Shigeyuki; Shimamoto, Kazuaki; Miura, Tetsuji.

In: Obesity, Vol. 23, No. 2, 01.02.2015, p. 359-367.

Research output: Contribution to journalArticle

TY - JOUR

T1 - FABP4 is secreted from adipocytes by adenyl cyclase-PKA- and guanylyl cyclase-PKG-dependent lipolytic mechanisms

AU - Mita, Tomohiro

AU - Furuhashi, Masato

AU - Hiramitsu, Shinya

AU - Ishii, Junichi

AU - Hoshina, Kyoko

AU - Ishimura, Shutaro

AU - Fuseya, Takahiro

AU - Watanabe, Yuki

AU - Tanaka, Marenao

AU - Ohno, Kohei

AU - Akasaka, Hiroshi

AU - Ohnishi, Hirofumi

AU - Yoshida, Hideaki

AU - Saitoh, Shigeyuki

AU - Shimamoto, Kazuaki

AU - Miura, Tetsuji

PY - 2015/2/1

Y1 - 2015/2/1

N2 - Objective Fatty acid-binding protein 4 (FABP4) is expressed in adipocytes, and elevated plasma FABP4 level is associated with obesity-mediated metabolic phenotype. Postprandial regulation and secretory signaling of FABP4 has been investigated. Methods Time courses of FABP4 levels were examined during an oral glucose tolerance test (OGTT; n = 53) or a high-fat test meal eating (n = 35). Effects of activators and inhibitors of adenyl cyclase (AC)-protein kinase A (PKA) signaling and guanylyl cyclase (GC)-protein kinase G (PKG) signaling on FABP4 secretion from mouse 3T3-L1 adipocytes were investigated. Results FABP4 level significantly declined after the OGTT or a high-fat meal eating, while insulin level was increased. Treatment with low and high glucose concentration or palmitate for 2 h did not affect FABP4 secretion from 3T3-L1 adipocytes. FABP4 secretion was increased by stimulation of lipolysis using isoproterenol, a β3-adrenoceptor agonist (CL316243), forskolin, dibutyryl-cAMP and atrial natriuretic peptide, and the induced FABP4 secretion was suppressed by insulin or an inhibitor of PKA (H-89), PKG (KT5823) or hormone sensitive lipase (CAY10499). Conclusions FABP4 is secreted from adipocytes in association with lipolysis regulated by AC-PKA- and GC-PKG-mediated signal pathways. Plasma FABP4 level declines postprandially, and suppression of FABP4 secretion by insulin-induced anti-lipolytic signaling may be involved in this decline in FABP4 level.

AB - Objective Fatty acid-binding protein 4 (FABP4) is expressed in adipocytes, and elevated plasma FABP4 level is associated with obesity-mediated metabolic phenotype. Postprandial regulation and secretory signaling of FABP4 has been investigated. Methods Time courses of FABP4 levels were examined during an oral glucose tolerance test (OGTT; n = 53) or a high-fat test meal eating (n = 35). Effects of activators and inhibitors of adenyl cyclase (AC)-protein kinase A (PKA) signaling and guanylyl cyclase (GC)-protein kinase G (PKG) signaling on FABP4 secretion from mouse 3T3-L1 adipocytes were investigated. Results FABP4 level significantly declined after the OGTT or a high-fat meal eating, while insulin level was increased. Treatment with low and high glucose concentration or palmitate for 2 h did not affect FABP4 secretion from 3T3-L1 adipocytes. FABP4 secretion was increased by stimulation of lipolysis using isoproterenol, a β3-adrenoceptor agonist (CL316243), forskolin, dibutyryl-cAMP and atrial natriuretic peptide, and the induced FABP4 secretion was suppressed by insulin or an inhibitor of PKA (H-89), PKG (KT5823) or hormone sensitive lipase (CAY10499). Conclusions FABP4 is secreted from adipocytes in association with lipolysis regulated by AC-PKA- and GC-PKG-mediated signal pathways. Plasma FABP4 level declines postprandially, and suppression of FABP4 secretion by insulin-induced anti-lipolytic signaling may be involved in this decline in FABP4 level.

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U2 - 10.1002/oby.20954

DO - 10.1002/oby.20954

M3 - Article

VL - 23

SP - 359

EP - 367

JO - Obesity

JF - Obesity

SN - 1930-7381

IS - 2

ER -