Changes of Fatty Acid Composition in Incubated Rat Pancreatic Islets

Martins, Edgair Fernandes; Miyasaka, Célio Kenji; Newsholme, Philip; Curi, Rui; Carpinelli, Ângelo Rafael

doi:10.1016/s1262-3636(07)70085-x

Cited by 30 publications

(34 citation statements)

References 36 publications

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“…However, enhanced ATP consumption resultant from initiation of cell defence mechanisms including activation of ion pumps and transporters will result in a critical fall in ATP levels, insulin secretion and finally apoptosis (Brownlee 2003). That the pro-inflammatory cytokine cocktail decreased b-cell triacylglycerol level was unexpected, indicating a shift towards fatty acid oxidation or export (Martins et al 2004). One possibility that might explain the functional impact of TAG hydrolysis in b cells is enhanced TAG/FA cycling stimulated by pro-inflammatory cytokine exposure.…”

Section: Discussionmentioning

confidence: 99%

Pro-inflammatory cytokines increase glucose, alanine and triacylglycerol utilization but inhibit insulin secretion in a clonal pancreatic β-cell line

Kiely

McClenaghan²,

Flatt³

et al. 2007

Journal of Endocrinology

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We have investigated the effects of prolonged exposure (24 h) to pro-inflammatory cytokines on b-cell metabolism and insulin secretion using clonal BRIN-BD11 b cells. Addition of IL-1b, tumour necrosis factor-a and IFN-g (at concentrations that did not induce apoptosis) inhibited chronic (24 h) and acute stimulated levels of insulin release (by 59 and 93% respectively), increased cellular glucose and alanine consumption, and also elevated lactate and glutamate release.However, ATP levels and cellular triacylglycerol were decreased while glutathione was increased. We conclude that sub-lethal concentrations of pro-inflammatory cytokines appear to shift b-cell metabolism away from a key role in energy generation and stimulus-secretion coupling and towards a catabolic state which may be related to cell defence.

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Section: Discussionmentioning

confidence: 99%

Pro-inflammatory cytokines increase glucose, alanine and triacylglycerol utilization but inhibit insulin secretion in a clonal pancreatic β-cell line

Kiely

McClenaghan²,

Flatt³

et al. 2007

Journal of Endocrinology

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“…2). In support of this, FFA release from islets in response to elevated glucose has been observed (99). While it seems likely that FFA signaling via FFAR1 involves increases in intracellular Ca 2ϩ , the mechanisms by which TG/FFA cycling provides signals for insulin secretion are poorly understood and are likely to be multiple.…”

Section: Fatty Acids and Insulin Secretionmentioning

confidence: 93%

Fatty Acid Signaling in the β-Cell and Insulin Secretion

Madiraju²,

et al. 2006

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Fatty acids (FAs) and other lipid molecules are important for many cellular functions, including vesicle exocytosis. For the pancreatic ␤-cell, while the presence of some FAs is essential for glucose-stimulated insulin secretion, FAs have enormous capacity to amplify glucose-stimulated insulin secretion, which is particularly operative in situations of ␤-cell compensation for insulin resistance. In this review, we propose that FAs do this via three interdependent processes, which we have assigned to a "trident model" of ␤-cell lipid signaling. The first two arms of the model implicate intracellular metabolism of FAs, whereas the third is related to membrane free fatty acid receptor (

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“…Determination of lipids and LPS in diets was performed using a method described previously (Martins et al, 2004). Briefly, fatty acids were derivatized with 4-bromomethyl-7-coumarin and the analysis performed in a Shimadzu model LC-10A liquid chromatographer.…”

Section: Antibodiesmentioning

confidence: 99%

Saturated Fatty Acids Produce an Inflammatory Response Predominantly through the Activation of TLR4 Signaling in Hypothalamus: Implications for the Pathogenesis of Obesity

Milanski¹,

Degasperi²,

Coope³

et al. 2009

J. Neurosci.

943

853

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In animal models of diet-induced obesity, the activation of an inflammatory response in the hypothalamus produces molecular and functional resistance to the anorexigenic hormones insulin and leptin. The primary events triggered by dietary fats that ultimately lead to hypothalamic cytokine expression and inflammatory signaling are unknown. Here, we test the hypothesis that dietary fats act through the activation of toll-like receptors 2/4 and endoplasmic reticulum stress to induce cytokine expression in the hypothalamus of rodents. According to our results, long-chain saturated fatty acids activate predominantly toll-like receptor 4 signaling, which determines not only the induction of local cytokine expression but also promotes endoplasmic reticulum stress. Rats fed on a monounsaturated fat-rich diet do not develop hypothalamic leptin resistance, whereas toll-like receptor 4 loss-of-function mutation and immunopharmacological inhibition of toll-like receptor 4 protects mice from diet-induced obesity. Thus, toll-like receptor 4 acts as a predominant molecular target for saturated fatty acids in the hypothalamus, triggering the intracellular signaling network that induces an inflammatory response, and determines the resistance to anorexigenic signals.

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Changes of Fatty Acid Composition in Incubated Rat Pancreatic Islets

Cited by 30 publications

References 36 publications

Pro-inflammatory cytokines increase glucose, alanine and triacylglycerol utilization but inhibit insulin secretion in a clonal pancreatic β-cell line

Pro-inflammatory cytokines increase glucose, alanine and triacylglycerol utilization but inhibit insulin secretion in a clonal pancreatic β-cell line

Fatty Acid Signaling in the β-Cell and Insulin Secretion

Saturated Fatty Acids Produce an Inflammatory Response Predominantly through the Activation of TLR4 Signaling in Hypothalamus: Implications for the Pathogenesis of Obesity

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