Nutritional Supplementation With<i>trans</i>-10,<i>cis</i>-12–Conjugated Linoleic Acid Induces Inflammation of White Adipose Tissue

Poirier, Hélène; Shapiro, Jennifer S.; Kim, Roy J.; Lazar, Mitchell A.

doi:10.2337/db06-0036

Cited by 170 publications

(185 citation statements)

References 43 publications

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“…A similar increase in TNF-a mRNA levels in response to t10c12-CLA treatment has also been reported in isolated adipocytes (21) . t10c12-CLA also enhanced TNF-a and IL-6 gene expression in white adipose tissue (22) , and increased TNF-a secretion in mouse splenocytes (23) . In porcine PBMC, the t10c12-CLAinduced enhancement of TNF-a production up-regulated the phagocytic capacity of porcine polymorphonuclear cells (24) .…”

Section: Discussionmentioning

confidence: 99%

“…t10c12-CLA increased TNF-a production through the activation of NF-kB in human adipocytes (27) . Moreover, t10c12-CLA directly induced IL-6 secretion in 3T3-L1 adipocytes by an NF-kB-dependent mechanism (22) . These observations indicate that t10c12-CLA may participate in the expression of inflammatory mediators through the activation of NF-kB.…”

Section: Discussionmentioning

confidence: 99%

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Trans-10,cis-12-conjugated linoleic acid modulates NF-κB activation and TNF-α production in porcine peripheral blood mononuclear cells via a PPARγ-dependent pathway

Kim

Kang

et al. 2010

Br J Nutr

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The activation of PPARg by ligands, including conjugated linoleic acid (CLA) isomers, plays an important role in the immune response. Among CLA isomers, trans-10, cis-12 (t10c12)-CLA is known to participate in the modulation of pro-inflammatory cytokine secretion. The aim of the present study was to assess the effect of t10c12-CLA on PPARg activation, NF-kB activation and TNF-a expression in lipopolysaccharide (LPS)-naive and LPS-stimulated porcine peripheral blood mononuclear cells (PBMC). In addition, the effect of PPARg inhibition on NF-kB activation and TNF-a expression in porcine PBMC was examined. t10c12-CLA was found to increase TNF-a expression and NF-kB activity in LPS-naive porcine PBMC. In contrast, t10c12-CLA decreased TNF-a expression and NF-kB activity in LPS-stimulated porcine PBMC. t10c12-CLA up-regulated PPARg activity and mRNA expression in both LPS-naive and LPS-stimulated porcine PBMC. GW9662, a PPARg antagonist, completely negated the modulating effects of t10c12-CLA on TNF-a expression and NF-kB activity in both LPS-naive and LPS-stimulated porcine PBMC. These results suggest that t10c12-CLA can modulate TNF-a production and NF-kB activation by a PPARg-dependent pathway in porcine PBMC.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Trans-10,cis-12-conjugated linoleic acid modulates NF-κB activation and TNF-α production in porcine peripheral blood mononuclear cells via a PPARγ-dependent pathway

Kim

Kang

et al. 2010

Br J Nutr

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“…CLA can cause resistance to insulin action by reducing plasma levels of adiponectin (80). The mRNA levels of adiponectin were reduced after CLA supplementation in rats (81) and in cultured human adipocyte cells (82). Since the adiponectin gene is modulated by activation of PPAR-g, suppression of the adiponectin gene can be partly attributed to the antagonistic effect of the trans-10, cis-12 CLA on PPAR-g (83).…”

Section: Effect Of Dietary Lipids On Circulating Adiponectin Levelsmentioning

confidence: 99%

Relationships between adiponectin levels, the metabolic syndrome, and type 2 diabetes: a literature review

Frankenberg

Reis

Gerchman

2017

Arch. Endocrinol. Metab.

116

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Elevated hepatic glucose production, impaired insulin secretion, and insulin resistance -abnormalities of glucose metabolism typically found in subjects with obesity -are major factors underlying the pathogenesis of type 2 diabetes (DM2) and the metabolic syndrome (MS). Adiponectin is a major regulator of glucose and lipid homeostasis via its insulin-sensitizing properties, and lower levels seems to be associated with the development of DM2 and MS. The purpose of this review is to clarify the mechanisms whereby adiponectin relates to the development of DM2 and MS and the association between polymorphisms of the adiponectin gene, circulating levels of the hormone, and its relationships with DM2. In addition, the impact of dietary lipids in the circulating levels of adiponectin will be addressed. According to the literature, circulating adiponectin levels seem to decrease as the number of MS components increases. Lower adiponectin concentrations are associated with higher intra-abdominal fat content. Therefore, adiponectin could link intra-abdominal fat with insulin resistance and development of MS. Therapeutic strategies that target the MS and its components, such as lifestyle modification through physical activity and weight loss, have been shown to increase adiponectin concentrations. Possible roles of diets containing either low or high amounts of fat, or different types of fat, have been analyzed in several studies, with heterogeneous results. Supplementation with n-3 PUFA modestly increases adiponectin levels, whereas conjugated linoleic acid supplementation appears to reduce concentrations when compared with unsaturated fatty acid supplementation used as an active placebo. Arch Endocrinol Metab. 2017;61(6):614-22

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“…Although a series of studies indicates that CLAs attenuate the development of impaired glucose tolerance and hyperinsulinemia (6,10,11), an at least equal number of studies support the notion that CLA intake is associated with serious adverse effects such as impaired insulin sensitivity, and ultimately, insulin resistance (8,12,13). Importantly, the molecular mechanisms underlying the effects of CLAs on glucose homeostasis are not completely understood.…”

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confidence: 99%

Conjugated Linoleic Acids Mediate Insulin Release through Islet G Protein-coupled Receptor FFA1/GPR40

Schmidt

Liebscher

Merten

et al. 2011

Journal of Biological Chemistry

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Among dietary components, conjugated linoleic acids (CLAs) have attracted considerable attention as weight loss supplements in the Western world because they reduce fat stores and increase muscle mass. However, a number of adverse effects are also ascribed to the intake of CLAs such as aggravation of insulin resistance and the risk of developing diabetes. However, the mechanisms accounting for the effects of CLAs on glucose homeostasis are incompletely understood. Herein we provide evidence that CLAs specifically activate the cell surface receptor FFA1, an emerging therapeutic target to treat type 2 diabetes. Using different recombinant cellular systems engineered to stably express FFA1 and a set of diverse functional assays including the novel, label-free non-invasive dynamic mass redistribution technology (Corning Epic biosensor), both CLA isomers cis-9, trans-11-CLA and trans-10, cis-12-CLA were found to activate FFA1 in vitro at concentrations sufficient to also account for FFA1 activation in vivo. Each CLA isomer markedly increased glucose-stimulated insulin secretion in insulin-producing INS-1E cells that endogenously express FFA1 and in primary pancreatic ␤-cells of wild type but not FFA1 ؊/؊ knock-out mice. Our findings establish a clear mechanistic link between CLAs and insulin production and identify the cell surface receptor FFA1 as a molecular target for CLAs, explaining their acute stimulatory effects on insulin secretion in vivo. CLAs are also revealed as insulinotropic components in widely used nutraceuticals, a finding with significant implication for development of FFA1 modulators to treat type 2 diabetes.

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Nutritional Supplementation Withtrans-10,cis-12–Conjugated Linoleic Acid Induces Inflammation of White Adipose Tissue

Cited by 170 publications

References 43 publications

Trans-10,cis-12-conjugated linoleic acid modulates NF-κB activation and TNF-α production in porcine peripheral blood mononuclear cells via a PPARγ-dependent pathway

Trans-10,cis-12-conjugated linoleic acid modulates NF-κB activation and TNF-α production in porcine peripheral blood mononuclear cells via a PPARγ-dependent pathway

Relationships between adiponectin levels, the metabolic syndrome, and type 2 diabetes: a literature review

Conjugated Linoleic Acids Mediate Insulin Release through Islet G Protein-coupled Receptor FFA1/GPR40

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