The regulation of adipogenesis through GPR120

Gotoh, Chizu; Hong, Yeon Hee; Iga, Tomoyo; Hishikawa, Daisuke; Suzuki, Yasuki; Song, Sung-Moo; Choi, Ki Choon; Adachi, Tomohiko; Hirasawa, Akira; Tsujimoto, Gozoh; Sasaki, Shin Ichi; Roh, Sang Gun

doi:10.1016/j.bbrc.2007.01.028

Cited by 216 publications

(190 citation statements)

References 16 publications

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“…Further studies are warranted to reconcile this controversy by measuring metabolic activities in the presence or absence of ADRB3 stimulation rather than UCP1 gene expression. There is a study showing that depletion of Ffar4 impairs white adipocyte differentiation (49). Therefore, it is plausible that white adipose tissue browning by n-3 PUFA might be a separate mechanism from augmented brown adipogenesis of classical brown fat.…”

Section: Discussionmentioning

confidence: 99%

Eicosapentaenoic Acid Potentiates Brown Thermogenesis through FFAR4-dependent Up-regulation of miR-30b and miR-378

Kim

Okla

Erickson

et al. 2016

Journal of Biological Chemistry

104

120

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Emerging evidence suggests that n-3 polyunsaturated fatty acids (PUFA) promote brown adipose tissue thermogenesis. However, the underlying mechanisms remain elusive. Here, we hypothesize that n-3 PUFA promotes brown adipogenesis by modulating miRNAs. To test this hypothesis, murine brown preadipocytes were induced to differentiate the fatty acids of palmitic, oleate, or eicosapentaenoic acid (EPA). The increases of brown-specific signature genes and oxygen consumption rate by EPA were concurrent with up-regulation of miR-30b and 378 but not by oleate or palmitic acid. Next, we hypothesize that free fatty acid receptor 4 (Ffar4), a functional receptor for n-3 PUFA, modulates miR-30b and 378. Treatment of Ffar4 agonist (GW9508) recapitulated the thermogenic activation of EPA by increasing oxygen consumption rate, brown-specific marker genes, and miR-30b and 378, which were abrogated in Ffar4-silenced cells. Intriguingly, addition of the miR-30b mimic was unable to restore EPA-induced Ucp1 expression in Ffar4-depleted cells, implicating that Ffar4 signaling activity is required for up-regulating the brown adipogenic program. Moreover, blockage of miR-30b or 378 by locked nucleic acid inhibitors significantly attenuated Ffar4 as well as brown-specific signature gene expression, suggesting the signaling interplay between Ffar4 and miR-30b/378. The association between miR-30b/378 and brown thermogenesis was also confirmed in fish oil-fed C57/BL6 mice. Interestingly, the Ffar4 agonism-mediated signaling axis of Ffar4-miR-30b/378-Ucp1 was linked with an elevation of cAMP in brown adipocytes, similar to cold-exposed or fish oil-fed brown fat. Taken together, our work identifies a novel function of Ffar4 in modulating brown adipogenesis partly through a mechanism involving cAMP activation and upregulation of miR-30b and miR-378.There are two specific types of fat with opposite functions, brown adipose tissue (BAT) 3 and white adipose tissue (WAT).WAT stores energy in the form of triglyceride, whereas BAT dissipates energy in the form of heat via uncoupling protein 1 (UCP1) (1). Recent advances in our understanding of BAT biology in humans have provided a new insight into weight loss strategies by boosting BAT thermogenesis. Despite the surge of research for identifying cellular and molecular regulators of brown fat development (2, 3), the role of dietary constituents, particularly dietary fatty acids (FA), in thermogenic activation is poorly understood. Depending on the degree of desaturation and the n-6/n-3 ratio, FA differentially control adiposity, insulin sensitivity, immune response (4), and probably energy expenditure (5-7). Lately, it has been suggested that n-3 polyunsaturated FA (PUFA) stimulate beige/brown adipogenesis in primary murine adipogenic precursor cells (5) as well as C57BL/6 mice (6, 7). The latter animal study suggests that n-3 PUFA are associated with sympathetic activation and increased ␤3-adrenergic receptor (Adrb3) signaling (7). However, the underlying mechanistic details of how dietary n-3 PUFA...

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Section: Discussionmentioning

confidence: 99%

Eicosapentaenoic Acid Potentiates Brown Thermogenesis through FFAR4-dependent Up-regulation of miR-30b and miR-378

Kim

Okla

Erickson

et al. 2016

Journal of Biological Chemistry

104

120

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“…In pancreatic beta cells, where FFAR1 is preferentially expressed, FFAR1 can directly mediate FFA-stimulated insulin secretion (Itoh et al 2003;Edfalk et al 2008;Janssen and Depoortere 2013). GPR120 is also a lipid receptor expressed in the taste buds, as well as in adipocytes and other cells (Gotoh et al 2007;Oh et al 2010;Janssen and Depoortere 2013). Recent studies have shown that GPR120 dysfunction leads to obesity, glucose intolerance, and fatty liver (Ichimura et al 2012;Janssen and Depoortere 2013;DiPatrizio 2014).…”

Section: Introductionmentioning

confidence: 99%

Association of Oral Fat Sensitivity with Body Mass Index, Taste Preference, and Eating Habits in Healthy Japanese Young Adults

Asano

Hong

Matsuyama

et al. 2016

Tohoku J. Exp. Med.

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Oral fat sensitivity (OFS, the ability to detect fat) may be related to overeating-induced obesity. However, it is largely unknown whether OFS affects taste preference and eating habits. Therefore, we aimed to evaluate (1) the association between body mass index (BMI) and OFS and (2) the relationship of OFS with four types of taste preference (sweet, sour, salty, and bitter) and eating habits using serial concentrations of oleic acid (OA) homogenized in non-fat milk and a self-reported questionnaire. Participants were 25 healthy Japanese individuals (mean age: 27.0 ± 5.6 years), among whom the OA detection threshold was significantly associated with BMI. Participants were divided into two subgroups based on oral sensitivity to 2.8 mM OA: hypersensitive (able to detect 2.8 mM OA, n = 16) and hyposensitive (unable to detect 2.8 mM OA, n = 9). The degree of sweet taste preference of the hypersensitive group was significantly higher than that of the hyposensitive group. Furthermore, there was significantly higher degree of preference for high-fat sweet foods than low-fat sweet foods in the hypersensitive group. There was also a significant inverse correlation between the OA detection threshold and the degree of both spare eating and postprandial satiety. Thus, OFS is associated not only with BMI, but also with the preference for high-fat sweet foods and eating habits. The present study provides novel insights that measuring OFS may be useful for assessing the risk of obesity associated with overeating in countries, including Japan, where BMI is increasing in the population.

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“…However, this is now thought to represent a pseudogene that is unlikely to be expressed as a functional protein [17]. GPR40 is abundantly expressed in pancreatic β-cells (see below) but GPR41 may be predominantly localised on immune cells [18] and GPR43 on adipocytes [19]. In addition to these molecules, certain structurally more divergent receptors whose ligands are free or derivatised fatty acids are encoded elsewhere in the genome, including GPR84, GPR119 and GPR120 [20][21][22].…”

Section: Introductionmentioning

confidence: 99%

G-protein coupled receptors mediating long chain fatty acid signalling in the pancreatic beta-cell

Morgan¹,

Dhayal²

2009

Biochemical Pharmacology

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It is increasingly clear that some of the effects of both free and derivatised long chain fatty acids in pancreatic beta-cells are mediated by a group of G-protein coupled receptors. Some of these display close structural homology while others are more divergent. This Commentary reviews the expression and functional roles of three such molecules, GPR40, GPR119 and GPR120. GPR40 is the best characterised of this group and appears to mediate the acute stimulatory effects of long chain fatty acids on insulin secretion. GPR40 has also been proposed as a potential mediator of fatty acid toxicity but this is more controversial. GPR119 is also involved in stimulation of insulin secretion and responds primarily to ethanolamine derivatives of long chain fatty acids and also to some lysophospholipids rather than to free fatty acids. It may represent a useful target for the development of new insulin secretagogues aimed to enhance insulin release in patients with type 2 diabetes. GPR120 is the most enigmatic of the lipid responsive cell-surface receptors and its function remains to be established. It has been proposed to play a cytoprotective role in certain other cell types but it is unclear whether it fulfils a similar function in beta-cells.

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The regulation of adipogenesis through GPR120

Cited by 216 publications

References 16 publications

Eicosapentaenoic Acid Potentiates Brown Thermogenesis through FFAR4-dependent Up-regulation of miR-30b and miR-378

Eicosapentaenoic Acid Potentiates Brown Thermogenesis through FFAR4-dependent Up-regulation of miR-30b and miR-378

Association of Oral Fat Sensitivity with Body Mass Index, Taste Preference, and Eating Habits in Healthy Japanese Young Adults

G-protein coupled receptors mediating long chain fatty acid signalling in the pancreatic beta-cell

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