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Ram Lochan Yadav - One of the best experts on this subject based on the ideXlab platform.

  • Somatic neural alterations in non-Diabetic Obesity: a cross-sectional study
    BMC Obesity, 2016
    Co-Authors: Ram Lochan Yadav, Deepak Sharma, Prakash Kumar Yadav, Dev Kumar Shah, Kopila Agrawal, Rita Khadka, Md. Nazrul Islam
    Abstract:

    Background Reports on alterations in somatic neural functions due to non-Diabetic Obesity, a major risk factor for diabetes, are few and still a matter of debate. Nevertheless, to our knowledge, reports lack any comments on the type of somatic nerve fibers affected in non-Diabetic Obesity. Therefore, this study aimed to find out the alteration in somatic neural functions in non-Diabetic obese persons if any. Methods The study was conducted on 30 adult non-Diabetic obese persons (mean age 32.07 ± 7.25 years) with BMI > 30 Kg/m^2 (mean BMI 30.02 ± 2.89 Kg/m^2) and 29 age- and sex-matched normal weight controls (mean age 30.48 ± 8.01 years) with BMI: 18–24Kg/m^2 (mean BMI 21.87 ± 2.40 Kg/m^2). Nerve conduction study (NCS) variables of median, tibial and sural nerves were assessed in each subject using standard protocol. The data were compared by Mann Whitney ‘U’ test. Results In comparison to normal weight persons, obese had lower compound muscle action potential (CMAP) amplitudes of right median [9.09(7.62–10.20) Vs 10.75(8.71–12.2) mV, p  = 0.025] and bilateral tibial nerves [Right: 8.5(7.04–11.18) Vs 12.1(10.55–15) mV, p  

  • Somatic neural alterations in non-Diabetic Obesity: a cross-sectional study
    BMC Obesity, 2016
    Co-Authors: Ram Lochan Yadav, Deepak Sharma, Prakash Kumar Yadav, Dev Kumar Shah, Kopila Agrawal, Rita Khadka, Nazrul Islam
    Abstract:

    Abstract Background Reports on alterations in somatic neural functions due to non-Diabetic Obesity, a major risk factor for diabetes, are few and still a matter of debate. Nevertheless, to our knowledge, reports lack any comments on the type of somatic nerve fibers affected in non-Diabetic Obesity. Therefore, this study aimed to find out the alteration in somatic neural functions in non-Diabetic obese persons if any. Methods The study was conducted on 30 adult non-Diabetic obese persons (mean age 32.07 ± 7.25 years) with BMI > 30 Kg/m 2 (mean BMI 30.02 ± 2.89 Kg/m 2 ) and 29 age- and sex-matched normal weight controls (mean age 30.48 ± 8.01 years) with BMI: 18–24Kg/m 2 (mean BMI 21.87 ± 2.40 Kg/m 2 ). Nerve conduction study (NCS) variables of median, tibial and sural nerves were assessed in each subject using standard protocol. The data were compared by Mann Whitney ‘U’ test. Results In comparison to normal weight persons, obese had lower compound muscle action potential (CMAP) amplitudes of right median [9.09(7.62–10.20) Vs 10.75(8.71–12.2) mV, p  = 0.025] and bilateral tibial nerves [Right: 8.5(7.04–11.18) Vs 12.1(10.55–15) mV, p p  = 0.002]. Furthermore, obese persons had prolonged CMAP durations of right and left median [10.5(9.62–12) Vs 10(8.4–10.3) ms, p  = 0.02 and 10.85(10–11.88) Vs 10(9–10.57) ms, p  = 0.019] and right tibial [10(9–11) 8.5(7.92–10) ms, p  = 0.032] nerves. Sensory NCS (sural nerve) also showed diminished sensory nerve action potential (SNAP) amplitude [16(12.08–18.21) vs 22.8(18.3–31.08) μV, p Conclusion This study documents subclinical peripheral nerve damage in non-Diabetic obese with abnormal NCS parameters; shorter amplitudes and prolonged CMAP and SNAP durations. The reduced amplitudes of mixed and sensory nerves might be due to decreased axonal number stimulation or actual decrease in number of axonal fibers, or defect at NMJ in non-Diabetic obese. Prolonged durations but normal onset latencies and conduction velocities strongly suggest involvement of slow conducting fibers.

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

  • Changes in cortical bone response to high-fat diet from adolescence to adulthood in mice
    Osteoporosis International, 2011
    Co-Authors: S. S. Ionova-martin, J. M. Wade, S. Tang, M. Shahnazari, J. W. Ager, N. E. Lane, W. Yao, T. Alliston, C. Vaisse, R. O. Ritchie
    Abstract:

    Diabetic Obesity is associated with increased fracture risk in adults and adolescents. We find in both adolescent and adult mice dramatically inferior mechanical properties and structural quality of cortical bone, in agreement with the human fracture data, although some aspects of the response to Obesity appear to differ by age. Introduction The association of Obesity with bone is complex and varies with age. Diabetic obese adolescents and adult humans have increased fracture risk. Prior studies have shown reduced mechanical properties as a result of high-fat diet (HFD) but do not fully address size-independent mechanical properties or structural quality, which are important to understand material behavior. Methods Cortical bone from femurs and tibiae from two age groups of C57BL/6 mice fed either HFD or low-fat diet (LFD) were evaluated for structural and bone turnover changes (SEM and histomorphometry) and tested for bending strength, bending stiffness, and fracture toughness. Leptin, IGF-I, and non-enzymatic glycation measurements were also collected. Results In both young and adult mice fed on HFD, femoral strength, stiffness, and toughness are all dramatically lower than controls. Inferior lamellar and osteocyte alignment also point to reduced structural quality in both age groups. Bone size was largely unaffected by HFD, although there was a shift from increasing bone size in obese adolescents to decreasing in adults. IGF-I levels were lower in young obese mice only. Conclusions While the response to Obesity of murine cortical bone mass, bone formation, and hormonal changes appear to differ by age, the bone mechanical properties for young and adult groups are similar. In agreement with human fracture trends, adult mice may be similarly susceptible to bone fracture to the young group, although cortical bone in the two age groups responds to Diabetic Obesity differently.

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

  • Effects of DSP-8658, a novel selective peroxisome proliferator-activated receptors a/γ modulator, on adipogenesis and glucose metabolism in Diabetic obese mice.
    Experimental and clinical endocrinology & diabetes : official journal German Society of Endocrinology [and] German Diabetes Association, 2015
    Co-Authors: T Goto, R Nakayama, M Yamanaka, M Takata, T Takazawa, K Watanabe, K Maruta, R Nagata, J Nagamine, A Tsuchida
    Abstract:

    Peroxisome proliferator-activated receptors (PPARs) play a key regulating role in homeostasis. In this study, we investigated the effects of DSP-8658, a novel selective PPARa/γ modulator, on adipogenesis and glucose metabolism in Diabetic obese mice and compared these effects to those of pioglitazone, a PPARγ full agonist. DSP-8658 functional activity was assessed by PPARγ-target genes expression in adipose 3T3-L1 cells and its anti-Diabetic efficacy evaluated in db/db mice. The effects of DSP-8658 on adipogenesis were investigated diet induced obese (DIO) KK-A(y) mice. DSP-8658 reduced the expression of PPARγ-target gene 11 beta hydroxysteroid dehydrogenase type 1 with an EC50 value 2.1-fold that of pioglitazone and 28.4-fold that of rosiglitazone. On the other hand, DSP-8658 increased the expression of fatty acid binding protein 4 and glycerol kinase genes with EC50 values 33-fold and >15-fold those of pioglitazone and 163-fold and >38-fold those of rosiglitazone, respectively. In db/db mice, DSP-8658, like pioglitazone, decreased blood glucose, HbA1c, and plasma triglyceride levels and increased plasma insulin concentration and pancreatic insulin contents. In DIO KK-A(y) mice, DSP-8658, unlike pioglitazone, decreased subcutaneous adipose tissue weight and mean adipocyte size. However, both DSP-8658 and pioglitazone improved blood glucose and HbA1c levels with similar efficacy. Although DSP-8658 did not change the expression levels of fatty acid transport protein 1 and glycerol kinase genes in subcutaneous adipose tissue of KK-A(y) mice, pioglitazone increased these gene expression levels. Unlike PPARγ full agonists, DSP-8658 ameliorates blood glucose without increasing adipogenesis in Diabetic Obesity mice. © Georg Thieme Verlag KG Stuttgart · New York.

  • Effects of DSP-8658, a novel selective peroxisome proliferator-activated receptors a/γ modulator, on adipogenesis and glucose metabolism in Diabetic obese mice.
    Experimental and Clinical Endocrinology & Diabetes, 2015
    Co-Authors: T Goto, R Nakayama, M Yamanaka, M Takata, T Takazawa, K Watanabe, K Maruta, R Nagata, J Nagamine, A Tsuchida
    Abstract:

    Aims/Introduction: Peroxisome proliferator-activated receptors (PPARs) play a key regulating role in homeostasis. In this study, we investigated the effects of DSP-8658, a novel selective PPARa/γ modulator, on adipogenesis and glucose metabolism in Diabetic obese mice and compared these effects to those of pioglitazone, a PPARγ full agonist. Materials and Methods: DSP-8658 functional activity was assessed by PPARγ-target genes expression in adipose 3T3-L1 cells and its anti-Diabetic efficacy evaluated in db/db mice. The effects of DSP-8658 on adipogenesis were investigated diet induced obese (DIO) KK-A y mice. Results: DSP-8658 reduced the expression of PPARγ-target gene 11 beta hydroxysteroid dehydrogenase type 1 with an EC 50 value 2.1-fold that of pioglitazone and 28.4-fold that of rosiglitazone. On the other hand, DSP-8658 increased the expression of fatty acid binding protein 4 and glycerol kinase genes with EC 50 values 33-fold and >15-fold those of pioglitazone and 163-fold and >38-fold those of rosiglitazone, respectively. In db/db mice, DSP-8658, like pioglitazone, decreased blood glucose, HbA1c, and plasma triglyceride levels and increased plasma insulin concentration and pancreatic insulin contents. In DIO KK-A y mice, DSP-8658, unlike pioglitazone, decreased subcutaneous adipose tissue weight and mean adipocyte size. However, both DSP-8658 and pioglitazone improved blood glucose and HbA1c levels with similar efficacy. Although DSP-8658 did not change the expression levels of fatty acid transport protein 1 and glycerol kinase genes in subcutaneous adipose tissue of KK-A y mice, pioglitazone increased these gene expression levels. Conclusion: Unlike PPARγ full agonists, DSP-8658 ameliorates blood glucose without increasing adipogenesis in Diabetic Obesity mice.

Md. Nazrul Islam - One of the best experts on this subject based on the ideXlab platform.

  • Somatic neural alterations in non-Diabetic Obesity: a cross-sectional study
    BMC Obesity, 2016
    Co-Authors: Ram Lochan Yadav, Deepak Sharma, Prakash Kumar Yadav, Dev Kumar Shah, Kopila Agrawal, Rita Khadka, Md. Nazrul Islam
    Abstract:

    Background Reports on alterations in somatic neural functions due to non-Diabetic Obesity, a major risk factor for diabetes, are few and still a matter of debate. Nevertheless, to our knowledge, reports lack any comments on the type of somatic nerve fibers affected in non-Diabetic Obesity. Therefore, this study aimed to find out the alteration in somatic neural functions in non-Diabetic obese persons if any. Methods The study was conducted on 30 adult non-Diabetic obese persons (mean age 32.07 ± 7.25 years) with BMI > 30 Kg/m^2 (mean BMI 30.02 ± 2.89 Kg/m^2) and 29 age- and sex-matched normal weight controls (mean age 30.48 ± 8.01 years) with BMI: 18–24Kg/m^2 (mean BMI 21.87 ± 2.40 Kg/m^2). Nerve conduction study (NCS) variables of median, tibial and sural nerves were assessed in each subject using standard protocol. The data were compared by Mann Whitney ‘U’ test. Results In comparison to normal weight persons, obese had lower compound muscle action potential (CMAP) amplitudes of right median [9.09(7.62–10.20) Vs 10.75(8.71–12.2) mV, p  = 0.025] and bilateral tibial nerves [Right: 8.5(7.04–11.18) Vs 12.1(10.55–15) mV, p  

Nazrul Islam - One of the best experts on this subject based on the ideXlab platform.

  • Somatic neural alterations in non-Diabetic Obesity: a cross-sectional study
    BMC Obesity, 2016
    Co-Authors: Ram Lochan Yadav, Deepak Sharma, Prakash Kumar Yadav, Dev Kumar Shah, Kopila Agrawal, Rita Khadka, Nazrul Islam
    Abstract:

    Abstract Background Reports on alterations in somatic neural functions due to non-Diabetic Obesity, a major risk factor for diabetes, are few and still a matter of debate. Nevertheless, to our knowledge, reports lack any comments on the type of somatic nerve fibers affected in non-Diabetic Obesity. Therefore, this study aimed to find out the alteration in somatic neural functions in non-Diabetic obese persons if any. Methods The study was conducted on 30 adult non-Diabetic obese persons (mean age 32.07 ± 7.25 years) with BMI > 30 Kg/m 2 (mean BMI 30.02 ± 2.89 Kg/m 2 ) and 29 age- and sex-matched normal weight controls (mean age 30.48 ± 8.01 years) with BMI: 18–24Kg/m 2 (mean BMI 21.87 ± 2.40 Kg/m 2 ). Nerve conduction study (NCS) variables of median, tibial and sural nerves were assessed in each subject using standard protocol. The data were compared by Mann Whitney ‘U’ test. Results In comparison to normal weight persons, obese had lower compound muscle action potential (CMAP) amplitudes of right median [9.09(7.62–10.20) Vs 10.75(8.71–12.2) mV, p  = 0.025] and bilateral tibial nerves [Right: 8.5(7.04–11.18) Vs 12.1(10.55–15) mV, p p  = 0.002]. Furthermore, obese persons had prolonged CMAP durations of right and left median [10.5(9.62–12) Vs 10(8.4–10.3) ms, p  = 0.02 and 10.85(10–11.88) Vs 10(9–10.57) ms, p  = 0.019] and right tibial [10(9–11) 8.5(7.92–10) ms, p  = 0.032] nerves. Sensory NCS (sural nerve) also showed diminished sensory nerve action potential (SNAP) amplitude [16(12.08–18.21) vs 22.8(18.3–31.08) μV, p Conclusion This study documents subclinical peripheral nerve damage in non-Diabetic obese with abnormal NCS parameters; shorter amplitudes and prolonged CMAP and SNAP durations. The reduced amplitudes of mixed and sensory nerves might be due to decreased axonal number stimulation or actual decrease in number of axonal fibers, or defect at NMJ in non-Diabetic obese. Prolonged durations but normal onset latencies and conduction velocities strongly suggest involvement of slow conducting fibers.