Incorporation of conjugated linoleic acid into brain lipids is not necessary for conjugated linoleic acid–induced reductions in feed intake or body fat in mice

Shelton, Valerie J.; Shelton, Abigail Grace; Azain, M. J.; Hargrave-Barnes, Kimberly M.

doi:10.1016/j.nutres.2012.10.003

Cited by 10 publications

(11 citation statements)

References 30 publications

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“…La elevada retención de CLA en el tejido adiposo y su alta correlación con la ingesta de ciertos ácidos grasos, como los AGPI e isómeros de AG (32), ha permitido que los niveles de estos AG en tejido adiposo, sean empleados como biomarcadores de consumo. En cerebro, no fueron detectados los isómeros, confirmando la alta resistencia y selectividad de este tejido reportada por Shelton (33). Así, estos resultados en su conjunto, confirman la incorporación preferencial de CLA en los tejidos ricos en lípidos neutros (34).…”

Section: Discussionunclassified

Efectos de los conjugados del ácido linoleico sobre la incorporación tisular de ácidos grasos y metabolismo lipídico en ratas deficientes en ácidos grasos esenciales

Fariña¹,

González²,

Latorre³

et al. 2014

FABICIB

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Section: Discussionunclassified

Efectos de los conjugados del ácido linoleico sobre la incorporación tisular de ácidos grasos y metabolismo lipídico en ratas deficientes en ácidos grasos esenciales

Fariña¹,

González²,

Latorre³

et al. 2014

FABICIB

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“…Furthermore, even when decreased food intake was observed, the reductions do not completely explain decreases in body fat (Shelton et al 2012;Hargrave et al 2002;Y. Park et al 2007;Miner et al 2001), suggesting favourable changes in body composition are independent of appetite control.…”

Section: Mechanisms Of Satietymentioning

confidence: 97%

“…Increased leptin concentrations was also reported after intracerebroventricular administration of CLA in rats, which decreased expression of NPY and AgRP and consequently feed intake (Cao et al 2007). However, another study rejected the idea that CLA affects neuropeptide expression in the hypothalamus, as no CLA isomers were identified in the brain (Shelton et al 2012). CLA did significantly decrease feed intake, but the authors suggest CLA may have altered serum hormone levels as opposed to a central mechanism.…”

Section: Leptinmentioning

confidence: 98%

Dietary lipids with potential to affect satiety: Mechanisms and evidence

Maher

Clegg

2018

Critical Reviews in Food Science and Nutrition

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Dietary fat has been implicated in the rise of obesity due to its energy density, palatability and weak effects on satiety. As fat is a major contributor to overall energy intake, incorporating fat with satiating properties could potentially reduce energy intake. This review outlines the potential mechanisms, as far as we know, by which Medium-Chain Triglycerides (MCT), Conjugated Linoleic Acid (CLA), Short-Chain Fatty Acids (SCFA), Diacylglycerol (DAG), n-3 PUFA, and Small Particle Lipids, exerts their satiating effects. The evidence suggests that the lipid with the most potential to enhance satiety is MCT. SCFA can also promote satiety, but oral administration has been linked to poor tolerability rather than satiety. Data on the appetite effects of CLA is limited but does suggest potential. Research comparing these lipids to each other is also lacking and should be explored to elucidate which of these 'functional lipids' is the most beneficial in enhancing satiety.

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“…The more efficient peroxismal β-oxidation of predominantly the t10,c12-CLA isomer might further account for the 3-fold higher concentration of the c9,t11-CLA isomer than that of the t10,c12-CLA isomer, which we found both in whole brain homogenates and in liver tissue. Although a direct application of CLAs into the cerebrospinal fluid decreased appetiteregulating neuropeptides [19], CLA incorporation into brain lipids by in vivo feeding does not correlate with changes in appetite-regulating neuropeptides and reductions in food intake [39]. We observed no change in food intake (data not shown) and in mRNA levels of NPY during CLA feeding (data not shown).…”

Section: Discussionmentioning

confidence: 65%

Mice Lacking Free Fatty Acid Receptor 1 (GPR40/FFAR1) are Protected Against Conjugated Linoleic Acid-Induced Fatty Liver but Develop Inflammation and Insulin Resistance in the Brain

Sartorius

Drescher

Panse

et al. 2015

Cell Physiol Biochem

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Background/Aims:Conjugated linoleic acids (CLAs) affect body fat distribution, induce insulin resistance and stimulate insulin secretion. The latter effect is mediated through the free fatty acid receptor-1 (GPR40/FFAR1). This study examines whether GPR40/FFAR1 interacts with tissue specific metabolic changes induced by CLAs. MethodsandResults:After chronic application of CLAs C57BL/6J wild type (WT) and GPR40/FFAR1 (Ffar1^-/-) knockout mice developed insulin resistance. Although CLAs accumulated in liver up to 46-fold genotype-independently, hepatic triglycerides augmented only in WT mice. This triglyceride deposition was not associated with increased inflammation. In contrast, in brain of CLA fed Ffar1^-/- mice mRNA levels of TNF-α were 2-fold higher than in brain of WT mice although CLAs accumulated genotype-independently in brain up to 4-fold. Concomitantly, Ffar1^-/- mice did not respond to intracerebroventricular (i.c.v.) insulin injection with an increase in cortical activity while WT mice reacted as assessed by radiotelemetric electrocorticography (ECoG) measurements. In vitro incubation of primary murine astrocytes confirmed that CLAs stimulate neuronal inflammation independent of GPR40/FFAR1. Conclusion:This study discloses that GPR40/FFAR1 indirectly modulates organ-specific effects of CLAs: the expression of functional GPR40/FFAR1 counteracts CLA-induced inflammation and insulin resistance in the brain, but favors the development of fatty liver.

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Incorporation of conjugated linoleic acid into brain lipids is not necessary for conjugated linoleic acid–induced reductions in feed intake or body fat in mice

Cited by 10 publications

References 30 publications

Efectos de los conjugados del ácido linoleico sobre la incorporación tisular de ácidos grasos y metabolismo lipídico en ratas deficientes en ácidos grasos esenciales

Efectos de los conjugados del ácido linoleico sobre la incorporación tisular de ácidos grasos y metabolismo lipídico en ratas deficientes en ácidos grasos esenciales

Dietary lipids with potential to affect satiety: Mechanisms and evidence

Mice Lacking Free Fatty Acid Receptor 1 (GPR40/FFAR1) are Protected Against Conjugated Linoleic Acid-Induced Fatty Liver but Develop Inflammation and Insulin Resistance in the Brain

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