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ffa-free-fatty-acid

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Meeting Abstracts
Journal: Diabetes
Diabetes 2018;67(Supplement_1):150-OR
Published: 01 July 2018
...ANNE-MARIE CARREAU; CHRISTOPHE NOLL; BRIGITTE GUERIN; LAURENT BIERTHO; ERIC E. TURCOTTE; ANDRE TCHERNOF; ANDRÉ CARPENTIER Postprandial dietary fatty acid (FA) biodistribution is impaired in subjects with glucose intolerance, with decreased FA storage in adipose tissues (AT) and increased FA uptake...
Meeting Abstracts
Journal: Diabetes
Diabetes 2020;69(Supplement_1):1881-P
Published: 01 June 2020
... and trained subjects were fasted overnight (Table1). To characterize muscle lipid turnover, we conducted a pulse-chase experiment using sequential [U-13C]palmitate and [9-2H]palmitate infusions (6 h each) with a 1 hour overlap to label endogenous and exogenous FFA pools. Biopsy#1 (Bx#1...
Meeting Abstracts
Journal: Diabetes
Diabetes 2019;68(Supplement_1):2427-PUB
Published: 01 June 2019
...AMEL REZKI; MARINOS FYSEKIDIS; EMMANUEL COSSON; PAUL VALENSI Objective: In diabetic patients, autonomic alterations are associated with hypertension. In healthy individuals, FFAs were shown to enhance sympathetic activity. We aimed to examine the influence of autonomic function alterations and FFA...
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A working model by which FGF21 maintains glucose homeostasis during fasting...
Published: 13 November 2014
Figure 8 A working model by which FGF21 maintains glucose homeostasis during fasting via mediating the cross talk between brain and liver. FFA, free fatty acids; HSL, hormone-sensitive lipase; TG, triglycerides. Figure 8. A working model by which FGF21 maintains glucose homeostasis during fastin... More
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Potential mechanisms by which intramuscular lipids impact insulin sensitivi...
Published: 13 April 2020
Figure 1 Potential mechanisms by which intramuscular lipids impact insulin sensitivity in skeletal muscle. AKT, protein kinase B; dhCer, dihydroceramide; FFA, free fatty acids; IRS-1, insulin receptor substrate-1; PKC, protein kinase C; PL, phospholipids; PP2A, protein phosphatase 2A; SPM, sphingo... More
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Liver glucose output can be regulated indirectly by afferent and efferent r...
Published: 12 October 2016
Liver glucose output can be regulated indirectly by afferent and efferent renal nerves by either central integration of afferent renal nerve signals, central insulin signaling, adrenergic control of adipose tissue lipolysis, or neurogenic control of the renin-angiotensin-aldosterone system (RAAS). F... More
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Working hypothesis. Overnutrition induces ER stress and inflammation in the...
Published: 14 May 2012
FIG. 1. Working hypothesis. Overnutrition induces ER stress and inflammation in the hypothalamus and activates downstream signaling effectors and processes such as IKK/NF-ĸB, JNK, and UPR to impair insulin and/or leptin signal transduction to activate KATP channels and inhibit hepatic glucose production. FFA, free fatty acid; PI3K, phosphatidylinostiol 3-kinase. FIG. 1. Working hypothesis. Overnutrition induces ER stress and inflammation in the hypothalamus and activates downstream signaling effectors and processes such as IKK/NF-ĸB, JNK, and UPR to impair insulin and/or leptin signal transduction to activate KATP channels and inhibit hepatic glucose production. FFA, free fatty acid; PI3K, phosphatidylinostiol 3-kinase. More
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Metformin, AMPK, and liver insulin resistance. Metformin-induced activation...
Published: 16 January 2018
Figure 2 Metformin, AMPK, and liver insulin resistance. Metformin-induced activation of AMPK in the liver suppresses de novo lipogenesis through phosphorylation and inhibition of ACC. Salsalate (a dimer of salicylate) also suppresses de novo lipogenesis by activating AMPK and inducing mitochondria... More
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Schematic of the TCA cycle, demonstrating incorporation of <sup>13</sup>C l...
Published: 01 May 2007
FIG. 1. Schematic of the TCA cycle, demonstrating incorporation of 13C label from plasma [2-13C]acetate into the muscle [4-13C]glutamate pool. *The carbon position labeled with 13C. Pyr, pyruvate; FFA, free fatty acids; AcCoA, acetyl-CoA; αKG, α-ketoglutarate. A single turn of the TCA cycle is shown; a second turn of the cycle forms [2-13C]glutamate and [3-13C]glutamate. FIG. 1. Schematic of the TCA cycle, demonstrating incorporation of 13C label from plasma [2-13C]acetate into the muscle [4-13C]glutamate pool. *The carbon position labeled with 13C. Pyr, pyruvate; FFA, free fatty acids; AcCoA, acetyl-CoA; αKG, α-ketoglutarate. A single turn of the TCA cycle is shown; a second turn of the cycle forms [2-13C]glutamate and [3-13C]glutamate. More
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Proposed model of the role of BIM in liver steatosis. In addition to its kn...
Published: 19 September 2017
Figure 7 Proposed model of the role of BIM in liver steatosis. In addition to its known function as a potent inducer of apoptosis, BIM is involved in regulation of mitochondrial activity and glucose homeostasis in hepatocytes. The present data clarify a novel mechanism by which obesity triggers ac... More
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Comparison of metabolic variables between subjects in the top (red bars) an...
Published: 16 November 2013
FIG. 4. Comparison of metabolic variables between subjects in the top (red bars) and bottom quartile (blue bars) of the distribution of the 12α-hydroxy/non–12α-hydroxy ratio in 200 nondiabetic subjects. Bar plots are median and interquartile range for the variables listed on the left-hand side. *0.05 ≥ P > 0.02; **0.02 ≥ P > 0.01, by Kruskal-Wallis test. FFA, free fatty acid; M/I, clamp-derived insulin sensitivity (in units of µmol ⋅ min−1 ⋅ kgffm−1 ⋅ nM−1). FIG. 4. Comparison of metabolic variables between subjects in the top (red bars) and bottom quartile (blue bars) of the distribution of the 12α-hydroxy/non–12α-hydroxy ratio in 200 nondiabetic subjects. Bar plots are median and interquartile range for the variables listed on the left-hand side. *0.05 ≥ P > 0.02; **0.02 ≥ P > 0.01, by Kruskal-Wallis test. FFA, free fatty acid; M/I, clamp-derived insulin sensitivity (in units of µmol ⋅ min−1 ⋅ kgffm−1 ⋅ nM−1). More
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Changes in metabolic flux adapted by the <em>fld</em> mouse during ...
Published: 01 December 2006
FIG. 7. Changes in metabolic flux adapted by the fld mouse during feeding and fasting. Metabolic flux through pathways in the wild-type mouse is illustrated by broken grey arrows. Only key changes in metabolic flux in the fld mouse are indicated by solid black arrows. The thickness of the black arrows indicates increased (thicker) or decreased (thinner) metabolic flux in the fld mouse, relative to the wild type. FFA, free fatty acids; G-6-P, glucose-6-phosphate; TG, triglyceride; WT, wild type. FIG. 7. Changes in metabolic flux adapted by the fld mouse during feeding and fasting. Metabolic flux through pathways in the wild-type mouse is illustrated by broken grey arrows. Only key changes in metabolic flux in the fld mouse are indicated by solid black arrows. The thickness of the black arrows indicates increased (thicker) or decreased (thinner) metabolic flux in the fld mouse, relative to the wild type. FFA, free fatty acids; G-6-P, glucose-6-phosphate; TG, triglyceride; WT, wild type. More
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CREBH is required to maintain rhythmic levels of lipids and FGF21. Levels o...
Published: 09 August 2016
Figure 5 CREBH is required to maintain rhythmic levels of lipids and FGF21. Levels of serum TG (A), serum free FA (B), hepatic TG (C), and serum FGF21 (D) in CREBH-null and WT mice under the circadian clock. Blood samples were collected every 6 h for 48 h in constant darkness to measure TG, FA, and FGF21 levels. Liver tissue samples of CREBH-null and WT control mice were collected every 4 h for 24 h in constant darkness to measure hepatic TG content. Data are mean ± SEM (n = 8 mice/time point). *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001. FFA, free fatty acid; KO, knockout. Figure 5. CREBH is required to maintain rhythmic levels of lipids and FGF21. Levels of serum TG (A), serum free FA (B), hepatic TG (C), and serum FGF21 (D) in CREBH-null and WT mice under the circadian clock. Blood samples were collected every 6 h for 48 h in constant darkness to measure TG, FA, and FGF21 levels. Liver tissue samples of CREBH-null and WT control mice were collected every 4 h for 24 h in constant darkness to measure hepatic TG content. Data are mean ± SEM (n = 8 mice/time point). *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001. FFA, free fatty acid; KO, knockout. More
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SirT1 transcript level is inversely correlated with macrophage markers in h...
Published: 13 November 2011
FIG. 6. SirT1 transcript level is inversely correlated with macrophage markers in human adults. A: Correlation between SirT1 mRNA expression and CD14 (a macrophage/monocyte marker) in adipose tissue of a mixed-weight population of humans. B: Correlation between SirT1 and CD86 mRNA (another monocyte/macrophage marker) in WAT from the same group of subjects. C: Correlation between SirT1 and CX3CL1 (a monocyte chemoattractant) mRNA in WAT from the same group of subjects. DF: SirT1 knockdown increases expression of CX3CL1, CX3CR1, and CD14 in rodent WAT. G: Schematic model of SirT1 regulation of inflammation. SirT1 deacetylation of inflammatory gene promoters causes decreased cytokine production in response to stimulation of inflammatory sensors by fatty acids, hypoxia, and ER stress. In turn, decreased SirT1 expression in obesity sensitizes these networks to activation by stressors. FFA, free fatty acid; NLR, NOD-like receptor. FIG. 6. SirT1 transcript level is inversely correlated with macrophage markers in human adults. A: Correlation between SirT1 mRNA expression and CD14 (a macrophage/monocyte marker) in adipose tissue of a mixed-weight population of humans. B: Correlation between SirT1 and CD86 mRNA (another monocyte/macrophage marker) in WAT from the same group of subjects. C: Correlation between SirT1 and CX3CL1 (a monocyte chemoattractant) mRNA in WAT from the same group of subjects. D–F: SirT1 knockdown increases expression of CX3CL1, CX3CR1, and CD14 in rodent WAT. G: Schematic model of SirT1 regulation of inflammation. SirT1 deacetylation of inflammatory gene promoters causes decreased cytokine production in response to stimulation of inflammatory sensors by fatty acids, hypoxia, and ER stress. In turn, decreased SirT1 expression in obesity sensitizes these networks to activation by stressors. FFA, free fatty acid; NLR, NOD-like receptor. More
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Metabolic effects of LXR. The figure shows a simplified model of potential ...
Published: 01 February 2004
FIG. 2. Metabolic effects of LXR. The figure shows a simplified model of potential regulatory mechanisms of LXR. See text for details. Blue arrows indicate stimulatory effects, whereas red arrows indicate inhibitory effects. LXR induces lipogenesis and inhibits hepatic gluconeogenesis. LXR reduces... More
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In silico analysis of Gpnmb expression reveals positive correlation with bo...
Published: 15 September 2014
Figure 1 In silico analysis of Gpnmb expression reveals positive correlation with body weight and negative correlation with insulin sensitivity measures. A: A Heatmap transformation of the correlation coefficients (P, Pearson; Rho; Spearman) of adipose Gpnmb expression to various metabolic traits scored in individuals from two independent mouse F2 intercrosses (BHF2 and CTB6F2). B: Example of correlation plot between adipose Gpnmb expression and body weight scored in BHF2 individuals. BMD, bone mineral density; FFA, free fatty acid; Glu, glucose; Ins, insulin; TC, total cholesterol; TG, triglyceride; UC, unesterified cholesterol. Figure 1. In silico analysis of Gpnmb expression reveals positive correlation with body weight and negative correlation with insulin sensitivity measures. A: A Heatmap transformation of the correlation coefficients (P, Pearson; Rho; Spearman) of adipose Gpnmb expression to various metabolic traits scored in individuals from two independent mouse F2 intercrosses (BHF2 and CTB6F2). B: Example of correlation plot between adipose Gpnmb expression and body weight scored in BHF2 individuals. BMD, bone mineral density; FFA, free fatty acid; Glu, glucose; Ins, insulin; TC, total cholesterol; TG, triglyceride; UC, unesterified cholesterol. More
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Metabolic effects of 2 weeks of acipimox treatment or placebo in T2D patien...
Published: 28 October 2014
Figure 2 Metabolic effects of 2 weeks of acipimox treatment or placebo in T2D patients. A: Effect of acipimox treatment for 2 weeks on plasma NEFA concentrations in T2D patients, both in the fasted state as during a hyperinsulinemic-euglycemic clamp. Dashed and solid arrows indicate the start of low (10 mU/m2/min) and high (40 mU/m2/min) infusion of insulin, respectively. B: WGD rates divided into oxidative glucose disposal and NOGD. C and D: EGP and skeletal muscle lipid content as measured by ORO staining in the vastus lateralis muscle. *P < 0.05. FFA, free fatty acid; ORO, oil red O. Figure 2. Metabolic effects of 2 weeks of acipimox treatment or placebo in T2D patients. A: Effect of acipimox treatment for 2 weeks on plasma NEFA concentrations in T2D patients, both in the fasted state as during a hyperinsulinemic-euglycemic clamp. Dashed and solid arrows indicate the start of low (10 mU/m2/min) and high (40 mU/m2/min) infusion of insulin, respectively. B: WGD rates divided into oxidative glucose disposal and NOGD. C and D: EGP and skeletal muscle lipid content as measured by ORO staining in the vastus lateralis muscle. *P < 0.05. FFA, free fatty acid; ORO, oil red O. More
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Molecular mechanism by which HFHSD leads to hepatic insulin resistance and ...
Published: 31 December 2014
Figure 5 Molecular mechanism by which HFHSD leads to hepatic insulin resistance and imeglimin’s action mode. A: HFHSD increases intracellular lipids (triglyceride and DAG), leading to alterations of mitochondrial function, which results in inhibition of insulin signaling. B: Imeglimin improves mitochondrial function by modulating mitochondrial lipid composition, increasing mitochondrial respiration associated with energy waste in succinate, decreasing ROS production, restoring CIII activity, decreasing CI activity, and reorienting oxidative fluxes to fatty acid oxidation. As a consequence, imeglimin leads to improved insulin signaling and decreased liver steatosis, insulin resistance, and glucose intolerance. CIV, complex IV; CoQ, coenzyme Q; CytC, cytochrome c; FADH2, flavin adenine dinucleotide; FFA, free fatty acid; IMM, inner mitochondrial membrane; IRS, insulin receptor substrate; JNK, Jun NH2-terminal kinase; mtDNA, mitochondrial DNA; OMM, outer mitochondrial membrane; PKC, protein kinase C; Ser-Thre, serine-threonine; TG, triglyceride. Figure 5. Molecular mechanism by which HFHSD leads to hepatic insulin resistance and imeglimin’s action mode. A: HFHSD increases intracellular lipids (triglyceride and DAG), leading to alterations of mitochondrial function, which results in inhibition of insulin signaling. B: Imeglimin improves mitochondrial function by modulating mitochondrial lipid composition, increasing mitochondrial respiration associated with energy waste in succinate, decreasing ROS production, restoring CIII activity, decreasing CI activity, and reorienting oxidative fluxes to fatty acid oxidation. As a consequence, imeglimin leads to improved insulin signaling and decreased liver steatosis, insulin resistance, and glucose intolerance. CIV, complex IV; CoQ, coenzyme Q; CytC, cytochrome c; FADH2, flavin adenine dinucleotide; FFA, free fatty acid; IMM, inner mitochondrial membrane; IRS, insulin receptor substrate; JNK, Jun NH2-terminal kinase; mtDNA, mitochondrial DNA; OMM, outer mitochondrial membrane; PKC, protein kinase C; Ser-Thre, serine-threonine; TG, triglyceride. More
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Caveolin-1 null mice show an impaired physiological response to fasting. ...
Published: 01 May 2004
FIG. 1. Caveolin-1 null mice show an impaired physiological response to fasting. A: Fasting increases the expression of caveolin-1 in the perigonadal fat pads of wild-type mice, as seen by Western blot analysis. B: Serum NEFA levels. The NEFA levels rise significantly in wild-type, but not caveolin-1 knockout, mice after a 48-h fast. Values represent the means ± SEM. FFA, free fatty acid. *P < 0.05 for caveolin-1 knockout vs. wild type; #P < 0.05 for wild type 48 h vs. 0 h. □, wild type; ▪, caveolin-1 knockout. FIG. 1. Caveolin-1 null mice show an impaired physiological response to fasting. A: Fasting increases the expression of caveolin-1 in the perigonadal fat pads of wild-type mice, as seen by Western blot analysis. B: Serum NEFA levels. The NEFA levels rise significantly in wild-type, but not caveolin-1 knockout, mice after a 48-h fast. Values represent the means ± SEM. FFA, free fatty acid. *P < 0.05 for caveolin-1 knockout vs. wild type; #P < 0.05 for wild type 48 h vs. 0 h. □, wild type; ▪, caveolin-1 knockout. More
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Schematic of skeletal muscle metabolite labeling after 1,6-<sup>13</sup>C...
Published: 01 July 2002
FIG. 1. Schematic of skeletal muscle metabolite labeling after 1,6-13C2 glucose precursor infusion. 13C label from glucose becomes incorporated into 1,6-13C2 glycogen and 3-13C pyruvate, which can be reduced to 3-13C lactate or converted to 3-13C alanine via aminotransferase reaction. The rate at which substrate enters the [lactate+pyruvate+alanine] pool is two times the glycolytic rate (2Vgly). The benefit of using the doubly labeled (1,6-13C2) glucose precursor is to double the 3-13C enrichment in lactate and alanine. α-kg, α-ketoglutarate; FFA, free fatty acid; Oaa, oxaloacetate; PDH, pyruvate dehydrogenase. FIG. 1. Schematic of skeletal muscle metabolite labeling after 1,6-13C2 glucose precursor infusion. 13C label from glucose becomes incorporated into 1,6-13C2 glycogen and 3-13C pyruvate, which can be reduced to 3-13C lactate or converted to 3-13C alanine via aminotransferase reaction. The rate at which substrate enters the [lactate+pyruvate+alanine] pool is two times the glycolytic rate (2Vgly). The benefit of using the doubly labeled (1,6-13C2) glucose precursor is to double the 3-13C enrichment in lactate and alanine. α-kg, α-ketoglutarate; FFA, free fatty acid; Oaa, oxaloacetate; PDH, pyruvate dehydrogenase. More