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Meeting Abstracts
Journal: Diabetes
Diabetes 2018;67(Supplement_1):2427-PUB
Published: 01 July 2018
... transport capacity during acute hyperglycemia in humans, which was also associated with higher total NEFA levels. Palmitic acid has been shown in vitro to suppress brain glucose uptake by downregulating GLUT1 expression in brain endothelial cells. Thus, this current study was undertaken...
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Altered brain–pancreas axis in <em>Syn-Foxo1<sup>−/−</sup></em> mic...
Published: 17 September 2013
FIG. 4. Altered brain–pancreas axis in Syn-Foxo1−/− mice. Glucose (A), insulin (B), and nonesterified fatty acid (C) levels after β3-adrenergic receptor agonist injection (n = 7 for each genotype). D: Insulin secretion from islets isolated from Syn-Foxo1 and wild-type mice (n = 8 for each genotype). Total/2,000: 1:2,000 dilution of islet insulin content obtained by acid extraction. E: Islet size quantification by morphometry (n = 6–8 for each genotype). F: Fasted and fed glucagon levels (n = 6–8 for each genotype). AU, arbitrary units; KO, knockout; NEFA, nonesterified fatty acid; WT, wild-type. *P < 0.05; **P < 0.01. FIG. 4. Altered brain–pancreas axis in Syn-Foxo1−/− mice. Glucose (A), insulin (B), and nonesterified fatty acid (C) levels after β3-adrenergic receptor agonist injection (n = 7 for each genotype). D: Insulin secretion from islets isolated from Syn-Foxo1 and wild-type mice (n = 8 for each genotype). Total/2,000: 1:2,000 dilution of islet insulin content obtained by acid extraction. E: Islet size quantification by morphometry (n = 6–8 for each genotype). F: Fasted and fed glucagon levels (n = 6–8 for each genotype). AU, arbitrary units; KO, knockout; NEFA, nonesterified fatty acid; WT, wild-type. *P < 0.05; **P < 0.01. More
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Fasting metabolic changes were attenuated in liver PTG<sup>OE</sup> animals...
Published: 02 October 2014
Figure 7 Fasting metabolic changes were attenuated in liver PTGOE animals. Control and liver PTGOE mice aged 6 weeks were fed a standard diet or an HFD for 16 weeks. Mice fasted for 16 h were killed. A: Fasting serum nonesterified fatty acids. B: Fasting serum β-hydroxybutyrate. C: Fasting liver triacylglycerol content. D: Lipid deposition as indicated by Oil Red O staining in liver sections from mice in the standard diet and HFD groups. Original magnification ×10. Data are mean ± SEM. n = 5–8/group. *P < 0.05 between control and PTGOE mice fed a standard diet or an HFD; #P < 0.05 between the standard diet and HFD. NEFA, nonesterified fatty acid; SD, standard diet. Figure 7. Fasting metabolic changes were attenuated in liver PTGOE animals. Control and liver PTGOE mice aged 6 weeks were fed a standard diet or an HFD for 16 weeks. Mice fasted for 16 h were killed. A: Fasting serum nonesterified fatty acids. B: Fasting serum β-hydroxybutyrate. C: Fasting liver triacylglycerol content. D: Lipid deposition as indicated by Oil Red O staining in liver sections from mice in the standard diet and HFD groups. Original magnification ×10. Data are mean ± SEM. n = 5–8/group. *P < 0.05 between control and PTGOE mice fed a standard diet or an HFD; #P < 0.05 between the standard diet and HFD. NEFA, nonesterified fatty acid; SD, standard diet. More
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Otop1<em><sup>tlt</sup></em> mutant mice develop more severe HFD-in...
Published: 13 March 2014
Figure 2 Otop1tlt mutant mice develop more severe HFD-induced insulin resistance. (A) Body weight of WT (open diamond; n = 8) and Otop1tlt mice (filled circle; n = 8) during HFD feeding. (B) Plasma concentrations of β-hydroxybutyrate, nonesterified fatty acids, and triglycerides after overnight fasting. (C) Plasma glucose and insulin levels under fed and fasted conditions. (D) Insulin tolerance test in WT (n = 6) and Otop1tlt (n = 7) mice in HFD-fed mice. (E) Glucose tolerance test in WT (n = 8) and Otop1tlt mice (n = 8) 9 weeks after HFD feeding. Data represent mean ± SEM. *P < 0.05, Otop1tlt vs. WT. NEFA, nonesterified fatty acids. Figure 2. Otop1tlt mutant mice develop more severe HFD-induced insulin resistance. (A) Body weight of WT (open diamond; n = 8) and Otop1tlt mice (filled circle; n = 8) during HFD feeding. (B) Plasma concentrations of β-hydroxybutyrate, nonesterified fatty acids, and triglycerides after overnight fasting. (C) Plasma glucose and insulin levels under fed and fasted conditions. (D) Insulin tolerance test in WT (n = 6) and Otop1tlt (n = 7) mice in HFD-fed mice. (E) Glucose tolerance test in WT (n = 8) and Otop1tlt mice (n = 8) 9 weeks after HFD feeding. Data represent mean ± SEM. *P < 0.05, Otop1tlt vs. WT. NEFA, nonesterified fatty acids. More
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BAT is activated upon cold exposure via the SNS. Thyroid hormones play an i...
Published: 07 June 2015
Figure 2 BAT is activated upon cold exposure via the SNS. Thyroid hormones play an important role in the upregulation of thermogenesis, and their local activity is dramatically increased by DIO2. Several peptide hormones have been demonstrated to induce differentiation of beige BAT in WAT depots i... More
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Metabolic changes of GIP or saline in euglycemic healthy overweight individ...
Published: 17 January 2012
FIG. 5. Metabolic changes of GIP or saline in euglycemic healthy overweight individuals (n = 11) relative to individual baseline value. A: Time course of GIP concentrations (P < 0.001). B: Time course of circulating insulin (P = N.S.). C: Time course of blood glucose levels (P = 0.028). D: Time course of FFAs (P = 0.046); NEFA, nonesterified fatty acid. E: Time course of free glycerol concentrations (P = N.S.). F: Time course of circulating triglycerides (P = N.S.). Data are mean ± SEM; P values are reported for treatment vs. time interaction (repeated-measures ANOVA). FIG. 5. Metabolic changes of GIP or saline in euglycemic healthy overweight individuals (n = 11) relative to individual baseline value. A: Time course of GIP concentrations (P < 0.001). B: Time course of circulating insulin (P = N.S.). C: Time course of blood glucose levels (P = 0.028). D: Time course of FFAs (P = 0.046); NEFA, nonesterified fatty acid. E: Time course of free glycerol concentrations (P = N.S.). F: Time course of circulating triglycerides (P = N.S.). Data are mean ± SEM; P values are reported for treatment vs. time interaction (repeated-measures ANOVA). More
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Recombinant FGF21 reduces plasma glucose, insulin, and lipid levels and imp...
Published: 01 January 2009
FIG. 2. Recombinant FGF21 reduces plasma glucose, insulin, and lipid levels and improves glucose tolerance in DIO mice. Mice were treated with vehicle or recombinant murine FGF21 intraperitonally at doses of 0 (vehicle), 0.1, 1, or 10 mg · kg−1 · day−1 divided into two daily injections (8:00 a.m. and 4:00 p.m.). Mice were fed ad libitum, and blood was collected 1 h after the morning injection on study day 24. A: Blood glucose. B: Plasma insulin. C: Plasma cholesterol and triglyceride levels. D: Plasma nonesterified free fatty acid (NFFA) levels. E: Plasma leptin. F: GTT was initiated 1 h after the morning injection on study day 30. Fasted mice were intraperitonally injected with 2 mg/kg glucose solution, and blood glucose was measured at 0 min (before glucose injection) and at 30 and 90 min (after glucose injection). Vehicle (open circles or open bars); FGF21 (open triangles or striped bars; 0.1, 1, and 10 denote FGF21 doses in mg · kg−1 · day−1); rosiglitazone (black squares or black bars). All data are means ± SE, n = 10 per group, ∧P < 0.05; #P < 0.01; *P < 0.001 vs. vehicle-treated high-fat diet mice. NEFA, nonesterified fatty acid. FIG. 2. Recombinant FGF21 reduces plasma glucose, insulin, and lipid levels and improves glucose tolerance in DIO mice. Mice were treated with vehicle or recombinant murine FGF21 intraperitonally at doses of 0 (vehicle), 0.1, 1, or 10 mg · kg−1 · day−1 divided into two daily injections (8:00 a.m. and 4:00 p.m.). Mice were fed ad libitum, and blood was collected 1 h after the morning injection on study day 24. A: Blood glucose. B: Plasma insulin. C: Plasma cholesterol and triglyceride levels. D: Plasma nonesterified free fatty acid (NFFA) levels. E: Plasma leptin. F: GTT was initiated 1 h after the morning injection on study day 30. Fasted mice were intraperitonally injected with 2 mg/kg glucose solution, and blood glucose was measured at 0 min (before glucose injection) and at 30 and 90 min (after glucose injection). Vehicle (open circles or open bars); FGF21 (open triangles or striped bars; 0.1, 1, and 10 denote FGF21 doses in mg · kg−1 · day−1); rosiglitazone (black squares or black bars). All data are means ± SE, n = 10 per group, ∧P < 0.05; #P < 0.01; *P < 0.001 vs. vehicle-treated high-fat diet mice. NEFA, nonesterified fatty acid. More
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Obese HXO mice are not protected against metabolic dysfunction. Obesity was...
Published: 01 April 2019
Figure 3 Obese HXO mice are not protected against metabolic dysfunction. Obesity was induced in HXO and FLX control mice through high-fat (41% kcal from fat) feeding for 26 weeks (n = 6 for all groups). Where indicated, age-matched lean WT mice were included as controls (n = 6 for all groups). A: Body weight progression. B: GTT during early (8–12 weeks of diet) and late (18–21 weeks of diet) stages of obesity. C: Plasma triglyceride (Tg), FFA, and insulin, and liver Tg at euthanasia. D: Lean and fat mass at early and late stages of obesity. E: VO2 and heat production at late stages of obesity. F: Activity and caloric intake at late stages of obesity. NEFA, nonesterified fatty acid. #P < 0.05 compared with WT lean; *P < 0.05 compared with obese FLX. Figure 3. Obese HXO mice are not protected against metabolic dysfunction. Obesity was induced in HXO and FLX control mice through high-fat (41% kcal from fat) feeding for 26 weeks (n = 6 for all groups). Where indicated, age-matched lean WT mice were included as controls (n = 6 for all groups). A: Body weight progression. B: GTT during early (8–12 weeks of diet) and late (18–21 weeks of diet) stages of obesity. C: Plasma triglyceride (Tg), FFA, and insulin, and liver Tg at euthanasia. D: Lean and fat mass at early and late stages of obesity. E: VO2 and heat production at late stages of obesity. F: Activity and caloric intake at late stages of obesity. NEFA, nonesterified fatty acid. #P < 0.05 compared with WT lean; *P < 0.05 compared with obese FLX. More
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Effects of rosiglitazone, Wy-14,643, or both rosiglitazone and Wy-14,643 tr...
Published: 01 December 2005
FIG. 1. Effects of rosiglitazone, Wy-14,643, or both rosiglitazone and Wy-14,643 treatment for 8 weeks on serum parameters and body weight in KKAy mice. Panels show blood glucose (A), fasting plasma insulin (B), fasting serum triglycerides (C), fasting NEFA (D), body weight (E), and food intake (F) of male KKAy mice treated with 0.01% rosiglitazone (rosi), 0.05% Wy-14,643 (Wy), or both 0.01% rosiglitazone and 0.05% Wy-14,643 (rosi+Wy) as food admixture for 8 weeks while on the high-fat diet. The same amount of food was given to the pair-fed group as to mice treated with Wy-14,643. Age-matched wild-type KK mice given normal chow were used as normal controls. Fasting parameters were measured after a 24-h fast. Each bar represents the means ± SE (n = 4 for pair-fed group, n = 6 for other groups). *P < 0.05; **P < 0.01. NEFA, nonesterified fatty acid; n.s., not significant. FIG. 1. Effects of rosiglitazone, Wy-14,643, or both rosiglitazone and Wy-14,643 treatment for 8 weeks on serum parameters and body weight in KKAy mice. Panels show blood glucose (A), fasting plasma insulin (B), fasting serum triglycerides (C), fasting NEFA (D), body weight (E), and food intake (F) of male KKAy mice treated with 0.01% rosiglitazone (rosi), 0.05% Wy-14,643 (Wy), or both 0.01% rosiglitazone and 0.05% Wy-14,643 (rosi+Wy) as food admixture for 8 weeks while on the high-fat diet. The same amount of food was given to the pair-fed group as to mice treated with Wy-14,643. Age-matched wild-type KK mice given normal chow were used as normal controls. Fasting parameters were measured after a 24-h fast. Each bar represents the means ± SE (n = 4 for pair-fed group, n = 6 for other groups). *P < 0.05; **P < 0.01. NEFA, nonesterified fatty acid; n.s., not significant. More
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Mechanistic models of lipid-induced impairment of muscle insulin action and...
Published: 01 November 2009
FIG. 4. Mechanistic models of lipid-induced impairment of muscle insulin action and supporting metabolomics data. Feeding of diets high in fat results in muscle insulin resistance, and recent studies suggest the operation of two possible mechanisms for this effect ( A ). A prevailing theory is that increased delivery of fat to muscle saturates the capacity for mitochondrial β-oxidation, leading to accumulation of bioactive lipid-derived metabolites such as diacylglycerols and ceramides in the extramitochondrial space and activation of stress/serine kinases that interfere with insulin action. More recent studies have shown that fatty acid oxidation is actually increased in muscle in response to high-fat feeding but with no coordinate increase in TCA cycle activity. This results in accumulation of incompletely oxidized lipids in the mitochondria and depletion of TCA cycle intermediates, possibly resulting in mitochondrial stress and interference with insulin actions. The metabolic changes that underpin this new mechanism were identified by targeted GC-MS of organic acids and MS-MS analysis of acylcarnitines in muscle extracts from lean and obese animals, as summarized in B (data reprinted from ref. 51 with permission). Note that these mechanisms are not mutually exclusive and could work in concert to impair muscle insulin action. CPT1, carnitine palmitoyltransferase 1; ETS, electron transport system; NEFA, nonesterified fatty acid; TCAI, TCA cycle intermediates. FIG. 4. Mechanistic models of lipid-induced impairment of muscle insulin action and supporting metabolomics data. Feeding of diets high in fat results in muscle insulin resistance, and recent studies suggest the operation of two possible mechanisms for this effect (A). A prevailing theory is that increased delivery of fat to muscle saturates the capacity for mitochondrial β-oxidation, leading to accumulation of bioactive lipid-derived metabolites such as diacylglycerols and ceramides in the extramitochondrial space and activation of stress/serine kinases that interfere with insulin action. More recent studies have shown that fatty acid oxidation is actually increased in muscle in response to high-fat feeding but with no coordinate increase in TCA cycle activity. This results in accumulation of incompletely oxidized lipids in the mitochondria and depletion of TCA cycle intermediates, possibly resulting in mitochondrial stress and interference with insulin actions. The metabolic changes that underpin this new mechanism were identified by targeted GC-MS of organic acids and MS-MS analysis of acylcarnitines in muscle extracts from lean and obese animals, as summarized in B (data reprinted from ref. 51 with permission). Note that these mechanisms are not mutually exclusive and could work in concert to impair muscle insulin action. CPT1, carnitine palmitoyltransferase 1; ETS, electron transport system; NEFA, nonesterified fatty acid; TCAI, TCA cycle intermediates. More
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Mechanistic models of lipid-induced impairment of muscle insulin action and...
Published: 01 November 2009
FIG. 4. Mechanistic models of lipid-induced impairment of muscle insulin action and supporting metabolomics data. Feeding of diets high in fat results in muscle insulin resistance, and recent studies suggest the operation of two possible mechanisms for this effect ( A ). A prevailing theory is that increased delivery of fat to muscle saturates the capacity for mitochondrial β-oxidation, leading to accumulation of bioactive lipid-derived metabolites such as diacylglycerols and ceramides in the extramitochondrial space and activation of stress/serine kinases that interfere with insulin action. More recent studies have shown that fatty acid oxidation is actually increased in muscle in response to high-fat feeding but with no coordinate increase in TCA cycle activity. This results in accumulation of incompletely oxidized lipids in the mitochondria and depletion of TCA cycle intermediates, possibly resulting in mitochondrial stress and interference with insulin actions. The metabolic changes that underpin this new mechanism were identified by targeted GC-MS of organic acids and MS-MS analysis of acylcarnitines in muscle extracts from lean and obese animals, as summarized in B (data reprinted from ref. 51 with permission). Note that these mechanisms are not mutually exclusive and could work in concert to impair muscle insulin action. CPT1, carnitine palmitoyltransferase 1; ETS, electron transport system; NEFA, nonesterified fatty acid; TCAI, TCA cycle intermediates. FIG. 4. Mechanistic models of lipid-induced impairment of muscle insulin action and supporting metabolomics data. Feeding of diets high in fat results in muscle insulin resistance, and recent studies suggest the operation of two possible mechanisms for this effect (A). A prevailing theory is that increased delivery of fat to muscle saturates the capacity for mitochondrial β-oxidation, leading to accumulation of bioactive lipid-derived metabolites such as diacylglycerols and ceramides in the extramitochondrial space and activation of stress/serine kinases that interfere with insulin action. More recent studies have shown that fatty acid oxidation is actually increased in muscle in response to high-fat feeding but with no coordinate increase in TCA cycle activity. This results in accumulation of incompletely oxidized lipids in the mitochondria and depletion of TCA cycle intermediates, possibly resulting in mitochondrial stress and interference with insulin actions. The metabolic changes that underpin this new mechanism were identified by targeted GC-MS of organic acids and MS-MS analysis of acylcarnitines in muscle extracts from lean and obese animals, as summarized in B (data reprinted from ref. 51 with permission). Note that these mechanisms are not mutually exclusive and could work in concert to impair muscle insulin action. CPT1, carnitine palmitoyltransferase 1; ETS, electron transport system; NEFA, nonesterified fatty acid; TCAI, TCA cycle intermediates. More
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Metabolic features of <em>Agrp-Gpr17<sup>−/−</sup></em> mice. <ital
Published: 15 July 2015
Figure 2 Metabolic features of Agrp-Gpr17−/− mice. A: Body weight (BW) of adult male WT and KO mice on chow diet (n = 25–30 for each genotype). The y-axis is limited to the range 20–40 g to better visualize individual differences. Body fat (B) and lean mass (C) in male mice analyzed by MRI (n = 15–16 for each genotype). In C, the y-axis is limited to the range 60–85% to better visualize individual differences. Serum leptin in ad libitum–fed (D), fasted (E), and refed (F) mice (n = 10–16 for each genotype). Serum glucose level after a short fast (G) (n = 18–21 for each genotype) or after overnight fasting (H) (n = 11–16 for each genotype). I: Serum fatty acids in ad libitum–fed mice (n = 22–31 for each genotype). Serum insulin after a short fast (J) (n = 18–22 for each genotype), an overnight fast (n = 12–16 for each genotype) (K), or refeeding (L) (n = 11–14 for each genotype). We present data as the mean ± SEM. *P < 0.05 (unpaired t test). NEFA, nonesterified fatty acid. Figure 2. Metabolic features of Agrp-Gpr17−/− mice. A: Body weight (BW) of adult male WT and KO mice on chow diet (n = 25–30 for each genotype). The y-axis is limited to the range 20–40 g to better visualize individual differences. Body fat (B) and lean mass (C) in male mice analyzed by MRI (n = 15–16 for each genotype). In C, the y-axis is limited to the range 60–85% to better visualize individual differences. Serum leptin in ad libitum–fed (D), fasted (E), and refed (F) mice (n = 10–16 for each genotype). Serum glucose level after a short fast (G) (n = 18–21 for each genotype) or after overnight fasting (H) (n = 11–16 for each genotype). I: Serum fatty acids in ad libitum–fed mice (n = 22–31 for each genotype). Serum insulin after a short fast (J) (n = 18–22 for each genotype), an overnight fast (n = 12–16 for each genotype) (K), or refeeding (L) (n = 11–14 for each genotype). We present data as the mean ± SEM. *P < 0.05 (unpaired t test). NEFA, nonesterified fatty acid. More
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Transgenic expression of Baf60c improves glucose metabolism in <em>ob/o</em>...
Published: 12 April 2014
Figure 8 Transgenic expression of Baf60c improves glucose metabolism in ob/ob mice. A: Fasting blood glucose and plasma insulin levels in ob/ob and ob/ob Tg mice, (n = five to seven mice per group). B: GTT and ITT in 4-month-old male mice (n = five to seven mice per group). C: Plasma levels of indicated metabolites from mice fasted overnight (n = five to seven mice per group). D: Immunoblots of total protein lysates from quadriceps muscle. E: Relative phosphorylation (p) levels of Akt on Thr308 and Ser473 residues in D after normalization to total (T) Akt levels. F: qPCR analysis of gene expression in quadriceps muscle. NEFA, nonesterified fatty acid; WT, wild-type. Values indicate mean ± SEM. All of the data shown are representative of at least three independent experiments. *P < 0.05 by two-tailed Student t test. Figure 8. Transgenic expression of Baf60c improves glucose metabolism in ob/ob mice. A: Fasting blood glucose and plasma insulin levels in ob/ob and ob/ob Tg mice, (n = five to seven mice per group). B: GTT and ITT in 4-month-old male mice (n = five to seven mice per group). C: Plasma levels of indicated metabolites from mice fasted overnight (n = five to seven mice per group). D: Immunoblots of total protein lysates from quadriceps muscle. E: Relative phosphorylation (p) levels of Akt on Thr308 and Ser473 residues in D after normalization to total (T) Akt levels. F: qPCR analysis of gene expression in quadriceps muscle. NEFA, nonesterified fatty acid; WT, wild-type. Values indicate mean ± SEM. All of the data shown are representative of at least three independent experiments. *P < 0.05 by two-tailed Student t test. More
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Four weeks of T2 administration prevents HFD-induced changes in systemic me...
Published: 17 October 2011
FIG. 1. Four weeks of T2 administration prevents HFD-induced changes in systemic metabolic parameters and fat accumulation, independently of TRβ. A: T2 normalizes HFD-altered metabolic parameters and B: glucose tolerance (upper) and insulin resistance (lower). Upper and lower insets: area under the curve (AUC). CF: T2 prevents fat (C) and triglyceride (D) accumulation and increases mitochondrial fatty acid oxidation (E) and phosphorylation of AMPK (Thr172) (F) in the indicated tissues. G: In contrast to T3, T2 does not activate the human uncoupling protein 3 promoter through interaction with TRβ in transiently transfected rat L6 myotubes. Error bars represent SEM. *P < 0.05 vs. untreated controls; **P < 0.05 vs. both untreated controls and HFD-fed groups; ***P < 0.05 vs. HFD-fed group. Energy efficiency = body weight gain/metabolized energy intake. BW, body weight; GW, gastrocnemius weight; LW, liver weight; NEFA, nonesterified fatty acids; prot, protein; VCO2, carbon dioxide production; WW, white adipose weight. Vo2 and energy expenditure are normalized to lean body weight. AE: □/◇ = N; ■ = HFD; ▨/△ = HFD-T2. G: ♦ = T2, △ = T3. (A high-quality color representation of this figure is available in the online issue.) FIG. 1. Four weeks of T2 administration prevents HFD-induced changes in systemic metabolic parameters and fat accumulation, independently of TRβ. A: T2 normalizes HFD-altered metabolic parameters and B: glucose tolerance (upper) and insulin resistance (lower). Upper and lower insets: area under the curve (AUC). C–F: T2 prevents fat (C) and triglyceride (D) accumulation and increases mitochondrial fatty acid oxidation (E) and phosphorylation of AMPK (Thr172) (F) in the indicated tissues. G: In contrast to T3, T2 does not activate the human uncoupling protein 3 promoter through interaction with TRβ in transiently transfected rat L6 myotubes. Error bars represent SEM. *P < 0.05 vs. untreated controls; **P < 0.05 vs. both untreated controls and HFD-fed groups; ***P < 0.05 vs. HFD-fed group. Energy efficiency = body weight gain/metabolized energy intake. BW, body weight; GW, gastrocnemius weight; LW, liver weight; NEFA, nonesterified fatty acids; prot, protein; VCO2, carbon dioxide production; WW, white adipose weight. Vo2 and energy expenditure are normalized to lean body weight. A–E: □/◇ = N; ■ = HFD; ▨/△ = HFD-T2. G: ♦ = T2, △ = T3. (A high-quality color representation of this figure is available in the online issue.) More
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Pharmacologic inhibition of XOR activity reverses HyUA in obesity but does ...
Published: 01 April 2019
Figure 4 Pharmacologic inhibition of XOR activity reverses HyUA in obesity but does not impact insulin sensitivity or lipid homeostasis. Obesity was induced in WT mice through high-fat (60% kcal from fat) feeding for 13 weeks. Mice were then continued on the same diet and treated with febuxostat (50 mg/L in drinking water) or vehicle (standard drinking water) for seven additional weeks (weeks 14–20). A: Body weight pre- and post-treatment (n = 5). B: Plasma triglyceride (Tg) and FFA, and liver Tg at euthanasia (n = 4–5). C: Relative tissue and absolute plasma XOR activity (left panels); relative tissue and absolute plasma UA concentration (right panels) (n = 8). DF: Data from euglycemic clamp studies (n = 5 all groups). D: Blood glucose and glucose infusion rate (GIR) time course. E: Endogenous glucose production (EGP) and plasma insulin. F: Basal and clamped glucose, GIR, and glucose uptake. AT, adipose tissue; Feb, febuxostat; KID, kidney; LIV, liver; MUS, muscle; NEFA, nonesterified fatty acid; Veh, vehicle. *P < 0.05 compared with obese vehicle. Figure 4. Pharmacologic inhibition of XOR activity reverses HyUA in obesity but does not impact insulin sensitivity or lipid homeostasis. Obesity was induced in WT mice through high-fat (60% kcal from fat) feeding for 13 weeks. Mice were then continued on the same diet and treated with febuxostat (50 mg/L in drinking water) or vehicle (standard drinking water) for seven additional weeks (weeks 14–20). A: Body weight pre- and post-treatment (n = 5). B: Plasma triglyceride (Tg) and FFA, and liver Tg at euthanasia (n = 4–5). C: Relative tissue and absolute plasma XOR activity (left panels); relative tissue and absolute plasma UA concentration (right panels) (n = 8). D–F: Data from euglycemic clamp studies (n = 5 all groups). D: Blood glucose and glucose infusion rate (GIR) time course. E: Endogenous glucose production (EGP) and plasma insulin. F: Basal and clamped glucose, GIR, and glucose uptake. AT, adipose tissue; Feb, febuxostat; KID, kidney; LIV, liver; MUS, muscle; NEFA, nonesterified fatty acid; Veh, vehicle. *P < 0.05 compared with obese vehicle. More
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Lipid homeostasis in the AS160<sup>R693X</sup> rats. <em>A</em> and...
Published: 12 May 2021
Figure 5 Lipid homeostasis in the AS160R693X rats. A and B: FA uptake (A) and oxidation (B) in soleus muscle isolated from the WT and AS160R693X rats. n = 7–8. CE: Cell surface and total CD36 levels in the WT and AS160R693X skeletal muscle (soleus) stimulated with or without insulin. C: Representative blots. D and E: Quantitative results of total (D) and cell surface (E) CD36 levels. n = 4. F and G: Serum TG (F) and FFA (G) levels after lipid administration via oral gavage in the WT and AS160R693X male rats at age 6–7 weeks. The values show the TG and FFA area under the curve (AUC) during a lipid tolerance test. n = 6–9. H: Expression of lipid metabolic genes in L6 muscle cell lines determined by QPCR. WT control and AS160-KD myocytes were transfected with a negative control siRNA (siNC) or an siRNA targeting CD36 (siCD36). n = 5. I: Schematic illustration of a model for regulation of PPARδ-dependent genes in skeletal muscle by the AS160-CD36 pathway. The AS160R684X mutation promotes CD36-mediated FA uptake into muscle cells, which consequently activates PPARδ and enhances transcription of its downstream target genes. The data are given as the mean ± SEM. *P < 0.05, **P < 0.01, and ***P < 0.001. NEFA, nonesterified fatty acids; p, phosphorylated. Figure 5. Lipid homeostasis in the AS160R693X rats. A and B: FA uptake (A) and oxidation (B) in soleus muscle isolated from the WT and AS160R693X rats. n = 7–8. C–E: Cell surface and total CD36 levels in the WT and AS160R693X skeletal muscle (soleus) stimulated with or without insulin. C: Representative blots. D and E: Quantitative results of total (D) and cell surface (E) CD36 levels. n = 4. F and G: Serum TG (F) and FFA (G) levels after lipid administration via oral gavage in the WT and AS160R693X male rats at age 6–7 weeks. The values show the TG and FFA area under the curve (AUC) during a lipid tolerance test. n = 6–9. H: Expression of lipid metabolic genes in L6 muscle cell lines determined by QPCR. WT control and AS160-KD myocytes were transfected with a negative control siRNA (siNC) or an siRNA targeting CD36 (siCD36). n = 5. I: Schematic illustration of a model for regulation of PPARδ-dependent genes in skeletal muscle by the AS160-CD36 pathway. The AS160R684X mutation promotes CD36-mediated FA uptake into muscle cells, which consequently activates PPARδ and enhances transcription of its downstream target genes. The data are given as the mean ± SEM. *P < 0.05, **P < 0.01, and ***P < 0.001. NEFA, nonesterified fatty acids; p, phosphorylated. More
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Effects of mild cold exposure on energy homeostasis and glucose tolerance. ...
Published: 12 March 2019
Figure 1 Effects of mild cold exposure on energy homeostasis and glucose tolerance. A: 5-week-old female mice were randomized to either a CD or WD at thermoneutrality (28°C) for 9 weeks. A third group of animals consumed a WD while housed under mild cold stress conditions (20°C) for 9 weeks. B: Weekly body weights (n = 5–8/group). C and D: Energy intake and metabolic efficiency (i.e., change in body weight over time per energy consumed) (n = 5–8/group). E: Average total EE (n = 5–8/group). F and G: Mean 24-h EE and spontaneous physical activity (SPA) curves (n = 5–8/group). H: Acute CTT. Baseline rectal temperature measurements were recorded in home cages (28°C or 20°C). Thereafter, mice were placed in environmental cold chambers (4°C) and rectal temperature measurements were taken every 30 min for 180 min (n = 5–8/group). I: Representative real-time thermal images captured during the CTT. Identical camera settings were used in ambient (home-cage temperature) and cold (4°C) environments. J: Plasma insulin concentrations (n = 5–8/group). K: GTT (n = 5–8/group). GTTs were performed at the same environmental temperature at which mice were housed. L: Plasma cholesterol and lipid concentrations (n = 5–8/group). Data are mean ± SE. *P < 0.05 vs. CD; #P < 0.05 vs. WD; ɸP < 0.05 CD vs. WD + mild cold. Chol, total cholesterol; d, day; HDLc, HDL cholesterol; LDLc, LDL cholesterol; NEFA, nonesterified fatty acid. Figure 1. Effects of mild cold exposure on energy homeostasis and glucose tolerance. A: 5-week-old female mice were randomized to either a CD or WD at thermoneutrality (28°C) for 9 weeks. A third group of animals consumed a WD while housed under mild cold stress conditions (20°C) for 9 weeks. B: Weekly body weights (n = 5–8/group). C and D: Energy intake and metabolic efficiency (i.e., change in body weight over time per energy consumed) (n = 5–8/group). E: Average total EE (n = 5–8/group). F and G: Mean 24-h EE and spontaneous physical activity (SPA) curves (n = 5–8/group). H: Acute CTT. Baseline rectal temperature measurements were recorded in home cages (28°C or 20°C). Thereafter, mice were placed in environmental cold chambers (4°C) and rectal temperature measurements were taken every 30 min for 180 min (n = 5–8/group). I: Representative real-time thermal images captured during the CTT. Identical camera settings were used in ambient (home-cage temperature) and cold (4°C) environments. J: Plasma insulin concentrations (n = 5–8/group). K: GTT (n = 5–8/group). GTTs were performed at the same environmental temperature at which mice were housed. L: Plasma cholesterol and lipid concentrations (n = 5–8/group). Data are mean ± SE. *P < 0.05 vs. CD; #P < 0.05 vs. WD; ɸP < 0.05 CD vs. WD + mild cold. Chol, total cholesterol; d, day; HDLc, HDL cholesterol; LDLc, LDL cholesterol; NEFA, nonesterified fatty acid. More
Images
Effects of voluntary exercise and low-fat diet on energy homeostasis and gl...
Published: 12 March 2019
Figure 4 Effects of voluntary exercise and low-fat diet on energy homeostasis and glucose tolerance in mice with diet-induced obesity. A: Experimental design. Five-week-old mice were fed a WD for 9 weeks. Thereafter, animals were allocated to one of the following groups: WD, WD+WR, and switched from a WD to a CD (n = 9–11/group). B and C: Weekly body weights and weekly running distance (n = 9–11/group). Running wheels were connected to a Sunding bicycle computer (SD-548B; Dongguan Sunding Electron Co., TangXia, DongGuan, China) for determination of weekly running distance. Odometers were checked daily and reset every week. D: Fat mass and lean mass via EchoMRI (n = 9–11/group). E: Organ/tissue weights (n = 9–11/group). F and G: Energy intake and metabolic efficiency (n = 9–11/group). H: Total EE assessed via metabolic cages. Data are presented as kcal/h/mouse (n = 8–11/group). I and J: Mean 24-h EE and spontaneous physical activity (SPA) tracings via metabolic chambers. Dark cycle is shaded in gray (n = 8–11/group). K: Acute CTT. Baseline rectal temperature measurements were recorded in home cages (28°C). Thereafter, mice were placed in environmental cold chambers (4°C) and rectal temperature measurements were taken every 30 min for 120 min (n = 5–9/group). L: GTT with glucose AUC (n = 9–11/group). M and N: Plasma insulin, cholesterol, and lipid concentrations (n = 8–10/group). Data are means ± SE. *P < 0.05 vs. WD; #P < 0.05 vs. WD+WR. BW, body weight; Chol, total cholesterol; d, day; HDLc, HDL cholesterol; LDLc, LDL cholesterol; NEFA, nonesterified fatty acid. Figure 4. Effects of voluntary exercise and low-fat diet on energy homeostasis and glucose tolerance in mice with diet-induced obesity. A: Experimental design. Five-week-old mice were fed a WD for 9 weeks. Thereafter, animals were allocated to one of the following groups: WD, WD+WR, and switched from a WD to a CD (n = 9–11/group). B and C: Weekly body weights and weekly running distance (n = 9–11/group). Running wheels were connected to a Sunding bicycle computer (SD-548B; Dongguan Sunding Electron Co., TangXia, DongGuan, China) for determination of weekly running distance. Odometers were checked daily and reset every week. D: Fat mass and lean mass via EchoMRI (n = 9–11/group). E: Organ/tissue weights (n = 9–11/group). F and G: Energy intake and metabolic efficiency (n = 9–11/group). H: Total EE assessed via metabolic cages. Data are presented as kcal/h/mouse (n = 8–11/group). I and J: Mean 24-h EE and spontaneous physical activity (SPA) tracings via metabolic chambers. Dark cycle is shaded in gray (n = 8–11/group). K: Acute CTT. Baseline rectal temperature measurements were recorded in home cages (28°C). Thereafter, mice were placed in environmental cold chambers (4°C) and rectal temperature measurements were taken every 30 min for 120 min (n = 5–9/group). L: GTT with glucose AUC (n = 9–11/group). M and N: Plasma insulin, cholesterol, and lipid concentrations (n = 8–10/group). Data are means ± SE. *P < 0.05 vs. WD; #P < 0.05 vs. WD+WR. BW, body weight; Chol, total cholesterol; d, day; HDLc, HDL cholesterol; LDLc, LDL cholesterol; NEFA, nonesterified fatty acid. More
Journal Articles
Journal: Diabetes
Diabetes 2005;54(9):2668–2673
Published: 01 September 2005
...). A triacylglycerol (TAG) stable isotope was added to the formula to determine the entry of dietary fatty acids into the serum and its clearance to the liver and resecretion into serum via VLDL. The contribution of dietary fatty acids to serum nonesterified fatty acids (NEFAs) was higher with meal feeding (24.4 ± 2.6...
Journal Articles
Journal: Diabetes
Diabetes 2005;54(9):2694–2701
Published: 01 September 2005
...Maureen T. Timlin; Brian R. Barrows; Elizabeth J. Parks Sources of fatty acids flowing to the liver may be used for triacylglycerol (TAG) synthesis. Our objective was to quantify contributions of nonesterified fatty acids (NEFAs), de novo lipogenesis, and dietary fatty acids to VLDL-TAG in the fed...