Reduced delta-6 desaturase activity partially protects against high-fat diet-induced impairment in whole-body glucose tolerance
Delta-6 desaturase (D6D), which is encoded by the fatty acid desaturase (Fads2) gene, is the rate-limiting enzyme for the endogenous production of n-3 long-chain polyunsaturated fatty acids. The absence of D6D activity in Fads2 −/− knockout mice results in the inability to produce eicosapentaenoic a...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Hucik, Barbora [verfasserIn] |
|---|
| Format: |
E-Artikel |
|---|---|
| Sprache: |
Englisch |
| Erschienen: |
2019transfer abstract |
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| Umfang: |
9 |
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| Übergeordnetes Werk: |
Enthalten in: Distribution of critical metals in evolving pyrite from massive sulfide ores of the Iberian Pyrite Belt - Yesares, Lola ELSEVIER, 2022, New York, NY [u.a.] |
|---|---|
| Übergeordnetes Werk: |
volume:67 ; year:2019 ; pages:173-181 ; extent:9 |
| Links: |
|---|
| DOI / URN: |
10.1016/j.jnutbio.2019.02.005 |
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ELV046695826 |
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| 520 | |a Delta-6 desaturase (D6D), which is encoded by the fatty acid desaturase (Fads2) gene, is the rate-limiting enzyme for the endogenous production of n-3 long-chain polyunsaturated fatty acids. The absence of D6D activity in Fads2 −/− knockout mice results in the inability to produce eicosapentaenoic acid and docosahexaenoic acid, and has previously been associated with altered glucose and lipid metabolism. Skeletal muscle is a major site for insulin-stimulated glucose disposal; however, the consequences of reduced D6D activity on skeletal muscle metabolism are unknown. The objective of this study was to examine the role of a partial reduction in D6D activity on whole-body glucose tolerance, skeletal muscle fatty acid profiles and protein content of key markers of carbohydrate and fat signaling pathways in the context of both low- and high-fat diets. Male C57BL/6J heterozygous (Fads2 +/− ) and wild-type (WT) mice were fed either a low-fat (16% kcal from fat) or high-fat (HFD; 45% kcal from fat) diet for 21 weeks. Fads2 +/− mice were protected from the HFD-induced impairment in glucose tolerance. Unexpectedly, HFD-fed Fads2 +/− mice had reduced GLUT4 skeletal muscle protein content compared to their WT counterparts. No changes were detected in total protein content of key markers of fatty acid uptake, glycogen formation or substrate oxidation. This study shows that reduced D6D activity is partially protective against HFD-induced impairments in whole-body glucose tolerance but does not appear to be due to increased muscle GLUT4 content or total content of proteins regulating substrate utilization. | ||
| 520 | |a Delta-6 desaturase (D6D), which is encoded by the fatty acid desaturase (Fads2) gene, is the rate-limiting enzyme for the endogenous production of n-3 long-chain polyunsaturated fatty acids. The absence of D6D activity in Fads2 −/− knockout mice results in the inability to produce eicosapentaenoic acid and docosahexaenoic acid, and has previously been associated with altered glucose and lipid metabolism. Skeletal muscle is a major site for insulin-stimulated glucose disposal; however, the consequences of reduced D6D activity on skeletal muscle metabolism are unknown. The objective of this study was to examine the role of a partial reduction in D6D activity on whole-body glucose tolerance, skeletal muscle fatty acid profiles and protein content of key markers of carbohydrate and fat signaling pathways in the context of both low- and high-fat diets. Male C57BL/6J heterozygous (Fads2 +/− ) and wild-type (WT) mice were fed either a low-fat (16% kcal from fat) or high-fat (HFD; 45% kcal from fat) diet for 21 weeks. Fads2 +/− mice were protected from the HFD-induced impairment in glucose tolerance. Unexpectedly, HFD-fed Fads2 +/− mice had reduced GLUT4 skeletal muscle protein content compared to their WT counterparts. No changes were detected in total protein content of key markers of fatty acid uptake, glycogen formation or substrate oxidation. This study shows that reduced D6D activity is partially protective against HFD-induced impairments in whole-body glucose tolerance but does not appear to be due to increased muscle GLUT4 content or total content of proteins regulating substrate utilization. | ||
| 700 | 1 | |a Sarr, Ousseynou |4 oth | |
| 700 | 1 | |a Nakamura, Manabu T. |4 oth | |
| 700 | 1 | |a Dyck, David J. |4 oth | |
| 700 | 1 | |a Mutch, David M. |4 oth | |
| 773 | 0 | 8 | |i Enthalten in |n Elsevier |a Yesares, Lola ELSEVIER |t Distribution of critical metals in evolving pyrite from massive sulfide ores of the Iberian Pyrite Belt |d 2022 |g New York, NY [u.a.] |w (DE-627)ELV009132147 |
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10.1016/j.jnutbio.2019.02.005 doi GBV00000000000615.pica (DE-627)ELV046695826 (ELSEVIER)S0955-2863(18)31172-0 DE-627 ger DE-627 rakwb eng 550 VZ 38.52 bkl 57.20 bkl Hucik, Barbora verfasserin aut Reduced delta-6 desaturase activity partially protects against high-fat diet-induced impairment in whole-body glucose tolerance 2019transfer abstract 9 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Delta-6 desaturase (D6D), which is encoded by the fatty acid desaturase (Fads2) gene, is the rate-limiting enzyme for the endogenous production of n-3 long-chain polyunsaturated fatty acids. The absence of D6D activity in Fads2 −/− knockout mice results in the inability to produce eicosapentaenoic acid and docosahexaenoic acid, and has previously been associated with altered glucose and lipid metabolism. Skeletal muscle is a major site for insulin-stimulated glucose disposal; however, the consequences of reduced D6D activity on skeletal muscle metabolism are unknown. The objective of this study was to examine the role of a partial reduction in D6D activity on whole-body glucose tolerance, skeletal muscle fatty acid profiles and protein content of key markers of carbohydrate and fat signaling pathways in the context of both low- and high-fat diets. Male C57BL/6J heterozygous (Fads2 +/− ) and wild-type (WT) mice were fed either a low-fat (16% kcal from fat) or high-fat (HFD; 45% kcal from fat) diet for 21 weeks. Fads2 +/− mice were protected from the HFD-induced impairment in glucose tolerance. Unexpectedly, HFD-fed Fads2 +/− mice had reduced GLUT4 skeletal muscle protein content compared to their WT counterparts. No changes were detected in total protein content of key markers of fatty acid uptake, glycogen formation or substrate oxidation. This study shows that reduced D6D activity is partially protective against HFD-induced impairments in whole-body glucose tolerance but does not appear to be due to increased muscle GLUT4 content or total content of proteins regulating substrate utilization. Delta-6 desaturase (D6D), which is encoded by the fatty acid desaturase (Fads2) gene, is the rate-limiting enzyme for the endogenous production of n-3 long-chain polyunsaturated fatty acids. The absence of D6D activity in Fads2 −/− knockout mice results in the inability to produce eicosapentaenoic acid and docosahexaenoic acid, and has previously been associated with altered glucose and lipid metabolism. Skeletal muscle is a major site for insulin-stimulated glucose disposal; however, the consequences of reduced D6D activity on skeletal muscle metabolism are unknown. The objective of this study was to examine the role of a partial reduction in D6D activity on whole-body glucose tolerance, skeletal muscle fatty acid profiles and protein content of key markers of carbohydrate and fat signaling pathways in the context of both low- and high-fat diets. Male C57BL/6J heterozygous (Fads2 +/− ) and wild-type (WT) mice were fed either a low-fat (16% kcal from fat) or high-fat (HFD; 45% kcal from fat) diet for 21 weeks. Fads2 +/− mice were protected from the HFD-induced impairment in glucose tolerance. Unexpectedly, HFD-fed Fads2 +/− mice had reduced GLUT4 skeletal muscle protein content compared to their WT counterparts. No changes were detected in total protein content of key markers of fatty acid uptake, glycogen formation or substrate oxidation. This study shows that reduced D6D activity is partially protective against HFD-induced impairments in whole-body glucose tolerance but does not appear to be due to increased muscle GLUT4 content or total content of proteins regulating substrate utilization. Sarr, Ousseynou oth Nakamura, Manabu T. oth Dyck, David J. oth Mutch, David M. oth Enthalten in Elsevier Yesares, Lola ELSEVIER Distribution of critical metals in evolving pyrite from massive sulfide ores of the Iberian Pyrite Belt 2022 New York, NY [u.a.] (DE-627)ELV009132147 volume:67 year:2019 pages:173-181 extent:9 https://doi.org/10.1016/j.jnutbio.2019.02.005 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OPC-GGO SSG-OPC-GEO 38.52 Geologie der Erze VZ 57.20 Exploration und Prospektion von Bodenschätzen VZ AR 67 2019 173-181 9 |
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10.1016/j.jnutbio.2019.02.005 doi GBV00000000000615.pica (DE-627)ELV046695826 (ELSEVIER)S0955-2863(18)31172-0 DE-627 ger DE-627 rakwb eng 550 VZ 38.52 bkl 57.20 bkl Hucik, Barbora verfasserin aut Reduced delta-6 desaturase activity partially protects against high-fat diet-induced impairment in whole-body glucose tolerance 2019transfer abstract 9 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Delta-6 desaturase (D6D), which is encoded by the fatty acid desaturase (Fads2) gene, is the rate-limiting enzyme for the endogenous production of n-3 long-chain polyunsaturated fatty acids. The absence of D6D activity in Fads2 −/− knockout mice results in the inability to produce eicosapentaenoic acid and docosahexaenoic acid, and has previously been associated with altered glucose and lipid metabolism. Skeletal muscle is a major site for insulin-stimulated glucose disposal; however, the consequences of reduced D6D activity on skeletal muscle metabolism are unknown. The objective of this study was to examine the role of a partial reduction in D6D activity on whole-body glucose tolerance, skeletal muscle fatty acid profiles and protein content of key markers of carbohydrate and fat signaling pathways in the context of both low- and high-fat diets. Male C57BL/6J heterozygous (Fads2 +/− ) and wild-type (WT) mice were fed either a low-fat (16% kcal from fat) or high-fat (HFD; 45% kcal from fat) diet for 21 weeks. Fads2 +/− mice were protected from the HFD-induced impairment in glucose tolerance. Unexpectedly, HFD-fed Fads2 +/− mice had reduced GLUT4 skeletal muscle protein content compared to their WT counterparts. No changes were detected in total protein content of key markers of fatty acid uptake, glycogen formation or substrate oxidation. This study shows that reduced D6D activity is partially protective against HFD-induced impairments in whole-body glucose tolerance but does not appear to be due to increased muscle GLUT4 content or total content of proteins regulating substrate utilization. Delta-6 desaturase (D6D), which is encoded by the fatty acid desaturase (Fads2) gene, is the rate-limiting enzyme for the endogenous production of n-3 long-chain polyunsaturated fatty acids. The absence of D6D activity in Fads2 −/− knockout mice results in the inability to produce eicosapentaenoic acid and docosahexaenoic acid, and has previously been associated with altered glucose and lipid metabolism. Skeletal muscle is a major site for insulin-stimulated glucose disposal; however, the consequences of reduced D6D activity on skeletal muscle metabolism are unknown. The objective of this study was to examine the role of a partial reduction in D6D activity on whole-body glucose tolerance, skeletal muscle fatty acid profiles and protein content of key markers of carbohydrate and fat signaling pathways in the context of both low- and high-fat diets. Male C57BL/6J heterozygous (Fads2 +/− ) and wild-type (WT) mice were fed either a low-fat (16% kcal from fat) or high-fat (HFD; 45% kcal from fat) diet for 21 weeks. Fads2 +/− mice were protected from the HFD-induced impairment in glucose tolerance. Unexpectedly, HFD-fed Fads2 +/− mice had reduced GLUT4 skeletal muscle protein content compared to their WT counterparts. No changes were detected in total protein content of key markers of fatty acid uptake, glycogen formation or substrate oxidation. This study shows that reduced D6D activity is partially protective against HFD-induced impairments in whole-body glucose tolerance but does not appear to be due to increased muscle GLUT4 content or total content of proteins regulating substrate utilization. Sarr, Ousseynou oth Nakamura, Manabu T. oth Dyck, David J. oth Mutch, David M. oth Enthalten in Elsevier Yesares, Lola ELSEVIER Distribution of critical metals in evolving pyrite from massive sulfide ores of the Iberian Pyrite Belt 2022 New York, NY [u.a.] (DE-627)ELV009132147 volume:67 year:2019 pages:173-181 extent:9 https://doi.org/10.1016/j.jnutbio.2019.02.005 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OPC-GGO SSG-OPC-GEO 38.52 Geologie der Erze VZ 57.20 Exploration und Prospektion von Bodenschätzen VZ AR 67 2019 173-181 9 |
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10.1016/j.jnutbio.2019.02.005 doi GBV00000000000615.pica (DE-627)ELV046695826 (ELSEVIER)S0955-2863(18)31172-0 DE-627 ger DE-627 rakwb eng 550 VZ 38.52 bkl 57.20 bkl Hucik, Barbora verfasserin aut Reduced delta-6 desaturase activity partially protects against high-fat diet-induced impairment in whole-body glucose tolerance 2019transfer abstract 9 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Delta-6 desaturase (D6D), which is encoded by the fatty acid desaturase (Fads2) gene, is the rate-limiting enzyme for the endogenous production of n-3 long-chain polyunsaturated fatty acids. The absence of D6D activity in Fads2 −/− knockout mice results in the inability to produce eicosapentaenoic acid and docosahexaenoic acid, and has previously been associated with altered glucose and lipid metabolism. Skeletal muscle is a major site for insulin-stimulated glucose disposal; however, the consequences of reduced D6D activity on skeletal muscle metabolism are unknown. The objective of this study was to examine the role of a partial reduction in D6D activity on whole-body glucose tolerance, skeletal muscle fatty acid profiles and protein content of key markers of carbohydrate and fat signaling pathways in the context of both low- and high-fat diets. Male C57BL/6J heterozygous (Fads2 +/− ) and wild-type (WT) mice were fed either a low-fat (16% kcal from fat) or high-fat (HFD; 45% kcal from fat) diet for 21 weeks. Fads2 +/− mice were protected from the HFD-induced impairment in glucose tolerance. Unexpectedly, HFD-fed Fads2 +/− mice had reduced GLUT4 skeletal muscle protein content compared to their WT counterparts. No changes were detected in total protein content of key markers of fatty acid uptake, glycogen formation or substrate oxidation. This study shows that reduced D6D activity is partially protective against HFD-induced impairments in whole-body glucose tolerance but does not appear to be due to increased muscle GLUT4 content or total content of proteins regulating substrate utilization. Delta-6 desaturase (D6D), which is encoded by the fatty acid desaturase (Fads2) gene, is the rate-limiting enzyme for the endogenous production of n-3 long-chain polyunsaturated fatty acids. The absence of D6D activity in Fads2 −/− knockout mice results in the inability to produce eicosapentaenoic acid and docosahexaenoic acid, and has previously been associated with altered glucose and lipid metabolism. Skeletal muscle is a major site for insulin-stimulated glucose disposal; however, the consequences of reduced D6D activity on skeletal muscle metabolism are unknown. The objective of this study was to examine the role of a partial reduction in D6D activity on whole-body glucose tolerance, skeletal muscle fatty acid profiles and protein content of key markers of carbohydrate and fat signaling pathways in the context of both low- and high-fat diets. Male C57BL/6J heterozygous (Fads2 +/− ) and wild-type (WT) mice were fed either a low-fat (16% kcal from fat) or high-fat (HFD; 45% kcal from fat) diet for 21 weeks. Fads2 +/− mice were protected from the HFD-induced impairment in glucose tolerance. Unexpectedly, HFD-fed Fads2 +/− mice had reduced GLUT4 skeletal muscle protein content compared to their WT counterparts. No changes were detected in total protein content of key markers of fatty acid uptake, glycogen formation or substrate oxidation. This study shows that reduced D6D activity is partially protective against HFD-induced impairments in whole-body glucose tolerance but does not appear to be due to increased muscle GLUT4 content or total content of proteins regulating substrate utilization. Sarr, Ousseynou oth Nakamura, Manabu T. oth Dyck, David J. oth Mutch, David M. oth Enthalten in Elsevier Yesares, Lola ELSEVIER Distribution of critical metals in evolving pyrite from massive sulfide ores of the Iberian Pyrite Belt 2022 New York, NY [u.a.] (DE-627)ELV009132147 volume:67 year:2019 pages:173-181 extent:9 https://doi.org/10.1016/j.jnutbio.2019.02.005 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OPC-GGO SSG-OPC-GEO 38.52 Geologie der Erze VZ 57.20 Exploration und Prospektion von Bodenschätzen VZ AR 67 2019 173-181 9 |
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10.1016/j.jnutbio.2019.02.005 doi GBV00000000000615.pica (DE-627)ELV046695826 (ELSEVIER)S0955-2863(18)31172-0 DE-627 ger DE-627 rakwb eng 550 VZ 38.52 bkl 57.20 bkl Hucik, Barbora verfasserin aut Reduced delta-6 desaturase activity partially protects against high-fat diet-induced impairment in whole-body glucose tolerance 2019transfer abstract 9 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Delta-6 desaturase (D6D), which is encoded by the fatty acid desaturase (Fads2) gene, is the rate-limiting enzyme for the endogenous production of n-3 long-chain polyunsaturated fatty acids. The absence of D6D activity in Fads2 −/− knockout mice results in the inability to produce eicosapentaenoic acid and docosahexaenoic acid, and has previously been associated with altered glucose and lipid metabolism. Skeletal muscle is a major site for insulin-stimulated glucose disposal; however, the consequences of reduced D6D activity on skeletal muscle metabolism are unknown. The objective of this study was to examine the role of a partial reduction in D6D activity on whole-body glucose tolerance, skeletal muscle fatty acid profiles and protein content of key markers of carbohydrate and fat signaling pathways in the context of both low- and high-fat diets. Male C57BL/6J heterozygous (Fads2 +/− ) and wild-type (WT) mice were fed either a low-fat (16% kcal from fat) or high-fat (HFD; 45% kcal from fat) diet for 21 weeks. Fads2 +/− mice were protected from the HFD-induced impairment in glucose tolerance. Unexpectedly, HFD-fed Fads2 +/− mice had reduced GLUT4 skeletal muscle protein content compared to their WT counterparts. No changes were detected in total protein content of key markers of fatty acid uptake, glycogen formation or substrate oxidation. This study shows that reduced D6D activity is partially protective against HFD-induced impairments in whole-body glucose tolerance but does not appear to be due to increased muscle GLUT4 content or total content of proteins regulating substrate utilization. Delta-6 desaturase (D6D), which is encoded by the fatty acid desaturase (Fads2) gene, is the rate-limiting enzyme for the endogenous production of n-3 long-chain polyunsaturated fatty acids. The absence of D6D activity in Fads2 −/− knockout mice results in the inability to produce eicosapentaenoic acid and docosahexaenoic acid, and has previously been associated with altered glucose and lipid metabolism. Skeletal muscle is a major site for insulin-stimulated glucose disposal; however, the consequences of reduced D6D activity on skeletal muscle metabolism are unknown. The objective of this study was to examine the role of a partial reduction in D6D activity on whole-body glucose tolerance, skeletal muscle fatty acid profiles and protein content of key markers of carbohydrate and fat signaling pathways in the context of both low- and high-fat diets. Male C57BL/6J heterozygous (Fads2 +/− ) and wild-type (WT) mice were fed either a low-fat (16% kcal from fat) or high-fat (HFD; 45% kcal from fat) diet for 21 weeks. Fads2 +/− mice were protected from the HFD-induced impairment in glucose tolerance. Unexpectedly, HFD-fed Fads2 +/− mice had reduced GLUT4 skeletal muscle protein content compared to their WT counterparts. No changes were detected in total protein content of key markers of fatty acid uptake, glycogen formation or substrate oxidation. This study shows that reduced D6D activity is partially protective against HFD-induced impairments in whole-body glucose tolerance but does not appear to be due to increased muscle GLUT4 content or total content of proteins regulating substrate utilization. Sarr, Ousseynou oth Nakamura, Manabu T. oth Dyck, David J. oth Mutch, David M. oth Enthalten in Elsevier Yesares, Lola ELSEVIER Distribution of critical metals in evolving pyrite from massive sulfide ores of the Iberian Pyrite Belt 2022 New York, NY [u.a.] (DE-627)ELV009132147 volume:67 year:2019 pages:173-181 extent:9 https://doi.org/10.1016/j.jnutbio.2019.02.005 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OPC-GGO SSG-OPC-GEO 38.52 Geologie der Erze VZ 57.20 Exploration und Prospektion von Bodenschätzen VZ AR 67 2019 173-181 9 |
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10.1016/j.jnutbio.2019.02.005 doi GBV00000000000615.pica (DE-627)ELV046695826 (ELSEVIER)S0955-2863(18)31172-0 DE-627 ger DE-627 rakwb eng 550 VZ 38.52 bkl 57.20 bkl Hucik, Barbora verfasserin aut Reduced delta-6 desaturase activity partially protects against high-fat diet-induced impairment in whole-body glucose tolerance 2019transfer abstract 9 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Delta-6 desaturase (D6D), which is encoded by the fatty acid desaturase (Fads2) gene, is the rate-limiting enzyme for the endogenous production of n-3 long-chain polyunsaturated fatty acids. The absence of D6D activity in Fads2 −/− knockout mice results in the inability to produce eicosapentaenoic acid and docosahexaenoic acid, and has previously been associated with altered glucose and lipid metabolism. Skeletal muscle is a major site for insulin-stimulated glucose disposal; however, the consequences of reduced D6D activity on skeletal muscle metabolism are unknown. The objective of this study was to examine the role of a partial reduction in D6D activity on whole-body glucose tolerance, skeletal muscle fatty acid profiles and protein content of key markers of carbohydrate and fat signaling pathways in the context of both low- and high-fat diets. Male C57BL/6J heterozygous (Fads2 +/− ) and wild-type (WT) mice were fed either a low-fat (16% kcal from fat) or high-fat (HFD; 45% kcal from fat) diet for 21 weeks. Fads2 +/− mice were protected from the HFD-induced impairment in glucose tolerance. Unexpectedly, HFD-fed Fads2 +/− mice had reduced GLUT4 skeletal muscle protein content compared to their WT counterparts. No changes were detected in total protein content of key markers of fatty acid uptake, glycogen formation or substrate oxidation. This study shows that reduced D6D activity is partially protective against HFD-induced impairments in whole-body glucose tolerance but does not appear to be due to increased muscle GLUT4 content or total content of proteins regulating substrate utilization. Delta-6 desaturase (D6D), which is encoded by the fatty acid desaturase (Fads2) gene, is the rate-limiting enzyme for the endogenous production of n-3 long-chain polyunsaturated fatty acids. The absence of D6D activity in Fads2 −/− knockout mice results in the inability to produce eicosapentaenoic acid and docosahexaenoic acid, and has previously been associated with altered glucose and lipid metabolism. Skeletal muscle is a major site for insulin-stimulated glucose disposal; however, the consequences of reduced D6D activity on skeletal muscle metabolism are unknown. The objective of this study was to examine the role of a partial reduction in D6D activity on whole-body glucose tolerance, skeletal muscle fatty acid profiles and protein content of key markers of carbohydrate and fat signaling pathways in the context of both low- and high-fat diets. Male C57BL/6J heterozygous (Fads2 +/− ) and wild-type (WT) mice were fed either a low-fat (16% kcal from fat) or high-fat (HFD; 45% kcal from fat) diet for 21 weeks. Fads2 +/− mice were protected from the HFD-induced impairment in glucose tolerance. Unexpectedly, HFD-fed Fads2 +/− mice had reduced GLUT4 skeletal muscle protein content compared to their WT counterparts. No changes were detected in total protein content of key markers of fatty acid uptake, glycogen formation or substrate oxidation. This study shows that reduced D6D activity is partially protective against HFD-induced impairments in whole-body glucose tolerance but does not appear to be due to increased muscle GLUT4 content or total content of proteins regulating substrate utilization. Sarr, Ousseynou oth Nakamura, Manabu T. oth Dyck, David J. oth Mutch, David M. oth Enthalten in Elsevier Yesares, Lola ELSEVIER Distribution of critical metals in evolving pyrite from massive sulfide ores of the Iberian Pyrite Belt 2022 New York, NY [u.a.] (DE-627)ELV009132147 volume:67 year:2019 pages:173-181 extent:9 https://doi.org/10.1016/j.jnutbio.2019.02.005 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OPC-GGO SSG-OPC-GEO 38.52 Geologie der Erze VZ 57.20 Exploration und Prospektion von Bodenschätzen VZ AR 67 2019 173-181 9 |
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reduced delta-6 desaturase activity partially protects against high-fat diet-induced impairment in whole-body glucose tolerance |
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Reduced delta-6 desaturase activity partially protects against high-fat diet-induced impairment in whole-body glucose tolerance |
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Delta-6 desaturase (D6D), which is encoded by the fatty acid desaturase (Fads2) gene, is the rate-limiting enzyme for the endogenous production of n-3 long-chain polyunsaturated fatty acids. The absence of D6D activity in Fads2 −/− knockout mice results in the inability to produce eicosapentaenoic acid and docosahexaenoic acid, and has previously been associated with altered glucose and lipid metabolism. Skeletal muscle is a major site for insulin-stimulated glucose disposal; however, the consequences of reduced D6D activity on skeletal muscle metabolism are unknown. The objective of this study was to examine the role of a partial reduction in D6D activity on whole-body glucose tolerance, skeletal muscle fatty acid profiles and protein content of key markers of carbohydrate and fat signaling pathways in the context of both low- and high-fat diets. Male C57BL/6J heterozygous (Fads2 +/− ) and wild-type (WT) mice were fed either a low-fat (16% kcal from fat) or high-fat (HFD; 45% kcal from fat) diet for 21 weeks. Fads2 +/− mice were protected from the HFD-induced impairment in glucose tolerance. Unexpectedly, HFD-fed Fads2 +/− mice had reduced GLUT4 skeletal muscle protein content compared to their WT counterparts. No changes were detected in total protein content of key markers of fatty acid uptake, glycogen formation or substrate oxidation. This study shows that reduced D6D activity is partially protective against HFD-induced impairments in whole-body glucose tolerance but does not appear to be due to increased muscle GLUT4 content or total content of proteins regulating substrate utilization. |
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Delta-6 desaturase (D6D), which is encoded by the fatty acid desaturase (Fads2) gene, is the rate-limiting enzyme for the endogenous production of n-3 long-chain polyunsaturated fatty acids. The absence of D6D activity in Fads2 −/− knockout mice results in the inability to produce eicosapentaenoic acid and docosahexaenoic acid, and has previously been associated with altered glucose and lipid metabolism. Skeletal muscle is a major site for insulin-stimulated glucose disposal; however, the consequences of reduced D6D activity on skeletal muscle metabolism are unknown. The objective of this study was to examine the role of a partial reduction in D6D activity on whole-body glucose tolerance, skeletal muscle fatty acid profiles and protein content of key markers of carbohydrate and fat signaling pathways in the context of both low- and high-fat diets. Male C57BL/6J heterozygous (Fads2 +/− ) and wild-type (WT) mice were fed either a low-fat (16% kcal from fat) or high-fat (HFD; 45% kcal from fat) diet for 21 weeks. Fads2 +/− mice were protected from the HFD-induced impairment in glucose tolerance. Unexpectedly, HFD-fed Fads2 +/− mice had reduced GLUT4 skeletal muscle protein content compared to their WT counterparts. No changes were detected in total protein content of key markers of fatty acid uptake, glycogen formation or substrate oxidation. This study shows that reduced D6D activity is partially protective against HFD-induced impairments in whole-body glucose tolerance but does not appear to be due to increased muscle GLUT4 content or total content of proteins regulating substrate utilization. |
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Delta-6 desaturase (D6D), which is encoded by the fatty acid desaturase (Fads2) gene, is the rate-limiting enzyme for the endogenous production of n-3 long-chain polyunsaturated fatty acids. The absence of D6D activity in Fads2 −/− knockout mice results in the inability to produce eicosapentaenoic acid and docosahexaenoic acid, and has previously been associated with altered glucose and lipid metabolism. Skeletal muscle is a major site for insulin-stimulated glucose disposal; however, the consequences of reduced D6D activity on skeletal muscle metabolism are unknown. The objective of this study was to examine the role of a partial reduction in D6D activity on whole-body glucose tolerance, skeletal muscle fatty acid profiles and protein content of key markers of carbohydrate and fat signaling pathways in the context of both low- and high-fat diets. Male C57BL/6J heterozygous (Fads2 +/− ) and wild-type (WT) mice were fed either a low-fat (16% kcal from fat) or high-fat (HFD; 45% kcal from fat) diet for 21 weeks. Fads2 +/− mice were protected from the HFD-induced impairment in glucose tolerance. Unexpectedly, HFD-fed Fads2 +/− mice had reduced GLUT4 skeletal muscle protein content compared to their WT counterparts. No changes were detected in total protein content of key markers of fatty acid uptake, glycogen formation or substrate oxidation. This study shows that reduced D6D activity is partially protective against HFD-induced impairments in whole-body glucose tolerance but does not appear to be due to increased muscle GLUT4 content or total content of proteins regulating substrate utilization. |
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