The Experts below are selected from a list of 360 Experts worldwide ranked by ideXlab platform

R Kluge - One of the best experts on this subject based on the ideXlab platform.

  • tbc1d1 mutation in lean mouse strain confers leanness and protects from Diet Induced Obesity
    Nature Genetics, 2008
    Co-Authors: Alexandra Chadt, Katja Leicht, Atul S Deshmukh, Lake Q Jiang, Stephan Scherneck, Ulrike Bernhardt, T Dreja, Heike Vogel, K Schmolz, R Kluge
    Abstract:

    Hadi Al-Hasani and colleagues report that a frameshift deletion in Tbc1d1 in lean SJL mice underlies a quantitative trait locus conferring protection against high-fat Diet-Induced Obesity. TBC1D1 seems to influence metabolism by regulating fatty acid uptake and oxidation in skeletal muscle cells. We previously identified Nob1 as a quantitative trait locus for high-fat Diet–Induced Obesity and diabetes in genome-wide scans of outcross populations of obese and lean mouse strains. Additional crossbreeding experiments indicated that Nob1 represents an Obesity suppressor from the lean Swiss Jim Lambert (SJL) strain. Here we identify a SJL-specific mutation in the Tbc1d1 gene that results in a truncated protein lacking the TBC Rab–GTPase-activating protein domain. TBC1D1, which has been recently linked to human Obesity, is related to the insulin signaling protein AS160 and is predominantly expressed in skeletal muscle. Knockdown of TBC1D1 in skeletal muscle cells increased fatty acid uptake and oxidation, whereas overexpression of TBC1D1 had the opposite effect. Recombinant congenic mice lacking TBC1D1 showed reduced body weight, decreased respiratory quotient, increased fatty acid oxidation and reduced glucose uptake in isolated skeletal muscle. Our data strongly suggest that mutation of Tbc1d1 suppresses high-fat Diet–Induced Obesity by increasing lipid use in skeletal muscle.

  • tbc1d1 mutation in lean mouse strain confers leanness and protects from Diet Induced Obesity
    Nature Genetics, 2008
    Co-Authors: Alexandra Chadt, Katja Leicht, Atul S Deshmukh, Lake Q Jiang, Stephan Scherneck, Ulrike Bernhardt, T Dreja, Heike Vogel, K Schmolz, R Kluge
    Abstract:

    Hadi Al-Hasani and colleagues report that a frameshift deletion in Tbc1d1 in lean SJL mice underlies a quantitative trait locus conferring protection against high-fat Diet-Induced Obesity. TBC1D1 seems to influence metabolism by regulating fatty acid uptake and oxidation in skeletal muscle cells.

Alexandra Chadt - One of the best experts on this subject based on the ideXlab platform.

  • tbc1d1 mutation in lean mouse strain confers leanness and protects from Diet Induced Obesity
    Nature Genetics, 2008
    Co-Authors: Alexandra Chadt, Katja Leicht, Atul S Deshmukh, Lake Q Jiang, Stephan Scherneck, Ulrike Bernhardt, T Dreja, Heike Vogel, K Schmolz, R Kluge
    Abstract:

    Hadi Al-Hasani and colleagues report that a frameshift deletion in Tbc1d1 in lean SJL mice underlies a quantitative trait locus conferring protection against high-fat Diet-Induced Obesity. TBC1D1 seems to influence metabolism by regulating fatty acid uptake and oxidation in skeletal muscle cells. We previously identified Nob1 as a quantitative trait locus for high-fat Diet–Induced Obesity and diabetes in genome-wide scans of outcross populations of obese and lean mouse strains. Additional crossbreeding experiments indicated that Nob1 represents an Obesity suppressor from the lean Swiss Jim Lambert (SJL) strain. Here we identify a SJL-specific mutation in the Tbc1d1 gene that results in a truncated protein lacking the TBC Rab–GTPase-activating protein domain. TBC1D1, which has been recently linked to human Obesity, is related to the insulin signaling protein AS160 and is predominantly expressed in skeletal muscle. Knockdown of TBC1D1 in skeletal muscle cells increased fatty acid uptake and oxidation, whereas overexpression of TBC1D1 had the opposite effect. Recombinant congenic mice lacking TBC1D1 showed reduced body weight, decreased respiratory quotient, increased fatty acid oxidation and reduced glucose uptake in isolated skeletal muscle. Our data strongly suggest that mutation of Tbc1d1 suppresses high-fat Diet–Induced Obesity by increasing lipid use in skeletal muscle.

  • tbc1d1 mutation in lean mouse strain confers leanness and protects from Diet Induced Obesity
    Nature Genetics, 2008
    Co-Authors: Alexandra Chadt, Katja Leicht, Atul S Deshmukh, Lake Q Jiang, Stephan Scherneck, Ulrike Bernhardt, T Dreja, Heike Vogel, K Schmolz, R Kluge
    Abstract:

    Hadi Al-Hasani and colleagues report that a frameshift deletion in Tbc1d1 in lean SJL mice underlies a quantitative trait locus conferring protection against high-fat Diet-Induced Obesity. TBC1D1 seems to influence metabolism by regulating fatty acid uptake and oxidation in skeletal muscle cells.

Katherine A Wilkinson - One of the best experts on this subject based on the ideXlab platform.

  • Diet Induced Obesity alters muscle spindle afferent function in adult mice
    PLOS ONE, 2018
    Co-Authors: Lubayna S Elahi, Krystle Shamai, Adam M Abtahie, Shreejit Padmanabhan, Martina Bremer, Katherine A Wilkinson
    Abstract:

    : Populations with Obesity are more likely to fall and exhibit balance instability. The reason for this is likely multifactorial, but there is some evidence that sensory function is impaired during Obesity. We tested the hypothesis that muscle proprioceptor function is compromised in a mouse model of Diet Induced Obesity. An in vitro muscle-nerve preparation was used to record muscle spindle afferent responses to physiological stretch and sinusoidal vibration. We compared the responses of C57/Bl6 male and female mice on a control Diet (10% kcal fat) with those eating a high fat Diet (HFD; 60% kcal fat) for 10 weeks (final age 14-15 weeks old). Following HFD feeding, adult mice of both sexes exhibited decreased muscle spindle afferent responses to muscle movement. Muscle spindle afferent firing rates during the plateau phase of stretch were significantly lower in both male and female HFD animals as were two measures of dynamic sensitivity (dynamic peak and dynamic index). Muscle spindle afferents in male mice on a HFD were also significantly less likely to entrain to vibration. Due to the importance of muscle spindle afferents to proprioception and motor control, decreased muscle spindle afferent responsiveness may contribute to balance instability during Obesity.

Stephan Scherneck - One of the best experts on this subject based on the ideXlab platform.

  • tbc1d1 mutation in lean mouse strain confers leanness and protects from Diet Induced Obesity
    Nature Genetics, 2008
    Co-Authors: Alexandra Chadt, Katja Leicht, Atul S Deshmukh, Lake Q Jiang, Stephan Scherneck, Ulrike Bernhardt, T Dreja, Heike Vogel, K Schmolz, R Kluge
    Abstract:

    Hadi Al-Hasani and colleagues report that a frameshift deletion in Tbc1d1 in lean SJL mice underlies a quantitative trait locus conferring protection against high-fat Diet-Induced Obesity. TBC1D1 seems to influence metabolism by regulating fatty acid uptake and oxidation in skeletal muscle cells. We previously identified Nob1 as a quantitative trait locus for high-fat Diet–Induced Obesity and diabetes in genome-wide scans of outcross populations of obese and lean mouse strains. Additional crossbreeding experiments indicated that Nob1 represents an Obesity suppressor from the lean Swiss Jim Lambert (SJL) strain. Here we identify a SJL-specific mutation in the Tbc1d1 gene that results in a truncated protein lacking the TBC Rab–GTPase-activating protein domain. TBC1D1, which has been recently linked to human Obesity, is related to the insulin signaling protein AS160 and is predominantly expressed in skeletal muscle. Knockdown of TBC1D1 in skeletal muscle cells increased fatty acid uptake and oxidation, whereas overexpression of TBC1D1 had the opposite effect. Recombinant congenic mice lacking TBC1D1 showed reduced body weight, decreased respiratory quotient, increased fatty acid oxidation and reduced glucose uptake in isolated skeletal muscle. Our data strongly suggest that mutation of Tbc1d1 suppresses high-fat Diet–Induced Obesity by increasing lipid use in skeletal muscle.

  • tbc1d1 mutation in lean mouse strain confers leanness and protects from Diet Induced Obesity
    Nature Genetics, 2008
    Co-Authors: Alexandra Chadt, Katja Leicht, Atul S Deshmukh, Lake Q Jiang, Stephan Scherneck, Ulrike Bernhardt, T Dreja, Heike Vogel, K Schmolz, R Kluge
    Abstract:

    Hadi Al-Hasani and colleagues report that a frameshift deletion in Tbc1d1 in lean SJL mice underlies a quantitative trait locus conferring protection against high-fat Diet-Induced Obesity. TBC1D1 seems to influence metabolism by regulating fatty acid uptake and oxidation in skeletal muscle cells.

Atul S Deshmukh - One of the best experts on this subject based on the ideXlab platform.

  • tbc1d1 mutation in lean mouse strain confers leanness and protects from Diet Induced Obesity
    Nature Genetics, 2008
    Co-Authors: Alexandra Chadt, Katja Leicht, Atul S Deshmukh, Lake Q Jiang, Stephan Scherneck, Ulrike Bernhardt, T Dreja, Heike Vogel, K Schmolz, R Kluge
    Abstract:

    Hadi Al-Hasani and colleagues report that a frameshift deletion in Tbc1d1 in lean SJL mice underlies a quantitative trait locus conferring protection against high-fat Diet-Induced Obesity. TBC1D1 seems to influence metabolism by regulating fatty acid uptake and oxidation in skeletal muscle cells. We previously identified Nob1 as a quantitative trait locus for high-fat Diet–Induced Obesity and diabetes in genome-wide scans of outcross populations of obese and lean mouse strains. Additional crossbreeding experiments indicated that Nob1 represents an Obesity suppressor from the lean Swiss Jim Lambert (SJL) strain. Here we identify a SJL-specific mutation in the Tbc1d1 gene that results in a truncated protein lacking the TBC Rab–GTPase-activating protein domain. TBC1D1, which has been recently linked to human Obesity, is related to the insulin signaling protein AS160 and is predominantly expressed in skeletal muscle. Knockdown of TBC1D1 in skeletal muscle cells increased fatty acid uptake and oxidation, whereas overexpression of TBC1D1 had the opposite effect. Recombinant congenic mice lacking TBC1D1 showed reduced body weight, decreased respiratory quotient, increased fatty acid oxidation and reduced glucose uptake in isolated skeletal muscle. Our data strongly suggest that mutation of Tbc1d1 suppresses high-fat Diet–Induced Obesity by increasing lipid use in skeletal muscle.

  • tbc1d1 mutation in lean mouse strain confers leanness and protects from Diet Induced Obesity
    Nature Genetics, 2008
    Co-Authors: Alexandra Chadt, Katja Leicht, Atul S Deshmukh, Lake Q Jiang, Stephan Scherneck, Ulrike Bernhardt, T Dreja, Heike Vogel, K Schmolz, R Kluge
    Abstract:

    Hadi Al-Hasani and colleagues report that a frameshift deletion in Tbc1d1 in lean SJL mice underlies a quantitative trait locus conferring protection against high-fat Diet-Induced Obesity. TBC1D1 seems to influence metabolism by regulating fatty acid uptake and oxidation in skeletal muscle cells.