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  • 1
    Online Resource
    Online Resource
    Adipocyte Differentiation-related Protein in Human Skeletal Muscle: Relationship to Insulin Sensitivity
    Wiley ; 2005
    In:  Obesity Research Vol. 13, No. 8 ( 2005-08), p. 1321-1329
    Details
    In: Obesity Research, Wiley, Vol. 13, No. 8 ( 2005-08), p. 1321-1329
    Type of Medium: Online Resource
    ISSN: 1071-7323
    URL: Article
    DOI: 10.1038/oby.2005.160
    Language: English
    Publisher: Wiley
    Publication Date: 2005
    detail.hit.zdb_id: 2027211-X
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  • 2
    Online Resource
    Online Resource
    Lack of Effect of Leptin on Glucose Transport, Lipoprotein Lipase, and Insulin Action in Adipose and Muscle Cells 1
    The Endocrine Society ; 1998
    In:  Endocrinology Vol. 139, No. 5 ( 1998-05), p. 2509-2513
    Details
    In: Endocrinology, The Endocrine Society, Vol. 139, No. 5 ( 1998-05), p. 2509-2513
    Type of Medium: Online Resource
    ISSN: 0013-7227 , 1945-7170
    URL: Article
    DOI: 10.1210/endo.139.5.5980
    Language: English
    Publisher: The Endocrine Society
    Publication Date: 1998
    detail.hit.zdb_id: 2011695-0
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  • 3
    Online Resource
    Online Resource
    Polycystic Ovary Syndrome Is Associated with Tissue-Specific Differences in Insulin Resistance
    The Endocrine Society ; 2009
    In:  The Journal of Clinical Endocrinology & Metabolism Vol. 94, No. 1 ( 2009-01-01), p. 157-163
    Details
    In: The Journal of Clinical Endocrinology & Metabolism, The Endocrine Society, Vol. 94, No. 1 ( 2009-01-01), p. 157-163
    Abstract: Objective: The potential differential contributions of skeletal muscle and adipose tissue to whole body insulin resistance were evaluated in subjects with polycystic ovary syndrome (PCOS). Research Design and Methods: Forty-two PCOS subjects and 15 body mass index-matched control subjects were studied. Insulin action was evaluated by the hyperinsulinemic/euglycemic clamp procedure. Isolated adipocytes and cultured muscle cells were analyzed for glucose transport activity; adipocytes, muscle tissue, and myotubes were analyzed for the expression and phosphorylation of insulin-signaling proteins. Results: Fifty-seven per cent of the PCOS subjects had impaired glucose tolerance and the lowest rate of maximal insulin-stimulated whole body glucose disposal compared to controls (P & lt; 0.01). PCOS subjects with normal glucose tolerance had intermediate reduction in glucose disposal rate (P & lt; 0.05 vs. both control and impaired glucose tolerance subjects). However, rates of maximal insulin-stimulated glucose transport (insulin responsiveness) into isolated adipocytes were comparable between all three groups, whereas PCOS subjects displayed impaired insulin sensitivity. In contrast, myotubes from PCOS subjects displayed reduced insulin responsiveness for glucose uptake and normal sensitivity. There were no differences between groups in the expression of glucose transporter 4 or insulin-signaling proteins or maximal insulin stimulation of phosphorylation of Akt in skeletal muscle, myotubes, or adipocytes. Conclusions: Individuals with PCOS display impaired insulin responsiveness in skeletal muscle and myotubes, whereas isolated adipocytes display impaired insulin sensitivity but normal responsiveness. Skeletal muscle and adipose tissue contribute differently to insulin resistance in PCOS. Insulin resistance in PCOS cannot be accounted for by differences in the expression of selected signaling molecules or maximal phosphorylation of Akt.
    Type of Medium: Online Resource
    ISSN: 0021-972X , 1945-7197
    URL: Article
    DOI: 10.1210/jc.2008-1492
    RVK:
    XA 10000
    Language: English
    Publisher: The Endocrine Society
    Publication Date: 2009
    detail.hit.zdb_id: 2026217-6
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  • 4
    Online Resource
    Online Resource
    Effects of the Rapid-Acting Insulin Analog Glulisine on Cultured Human Skeletal Muscle Cells: Comparisons with Insulin and Insulin-Like Growth Factor I
    The Endocrine Society ; 2005
    In:  The Journal of Clinical Endocrinology & Metabolism Vol. 90, No. 10 ( 2005-10), p. 5551-5558
    Details
    In: The Journal of Clinical Endocrinology & Metabolism, The Endocrine Society, Vol. 90, No. 10 ( 2005-10), p. 5551-5558
    Type of Medium: Online Resource
    ISSN: 0021-972X , 1945-7197
    URL: Article
    DOI: 10.1210/jc.2005-1007
    RVK:
    XA 10000
    Language: English
    Publisher: The Endocrine Society
    Publication Date: 2005
    detail.hit.zdb_id: 2026217-6
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  • 5
    Online Resource
    Online Resource
    Thiazolidinediones upregulate impaired fatty acid uptake in skeletal muscle of type 2 diabetic subjects
    American Physiological Society ; 2003
    In:  American Journal of Physiology-Endocrinology and Metabolism Vol. 285, No. 2 ( 2003-08), p. E354-E362
    Details
    In: American Journal of Physiology-Endocrinology and Metabolism, American Physiological Society, Vol. 285, No. 2 ( 2003-08), p. E354-E362
    Abstract: We examined the regulation of free fatty acid (FFA, palmitate) uptake into skeletal muscle cells of nondiabetic and type 2 diabetic subjects. Palmitate uptake included a protein-mediated component that was inhibited by phloretin. The protein-mediated component of uptake in muscle cells from type 2 diabetic subjects (78 ± 13 nmol · mg protein - 1 · min - 1 ) was reduced compared with that in nondiabetic muscle (150 ± 17, P 〈 0.01). Acute insulin exposure caused a modest (16 ± 5%, P 〈 0.025) but significant increase in protein-mediated uptake in nondiabetic muscle. There was no significant insulin effect in diabetic muscle (+19 ± 19%, P = not significant). Chronic (4 day) treatment with a series of thiazolidinediones, troglitazone (Tgz), rosiglitazone (Rgz), and pioglitazone (Pio) increased FFA uptake. Only the phloretin-inhibitable component was increased by treatment, which normalized this activity in diabetic muscle cells. Under the same conditions, FFA oxidation was also increased by thiazolidinedione treatment. Increases in FFA uptake and oxidation were associated with upregulation of fatty acid translocase (FAT/CD36) expression. FAT/CD36 protein was increased by Tgz (90 ± 22% over control), Rgz (146 ± 42%), and Pio (111 ± 37%, P 〈 0.05 for all 3) treatment. Tgz treatment had no effect on fatty acid transporter protein-1 and membrane-associated plasmalemmal fatty acid-binding protein mRNA expression. We conclude that FFA uptake into cultured muscle cells is, in part, protein mediated and acutely insulin responsive. The basal activity of FFA uptake is impaired in type 2 diabetes. In addition, chronic thiazolidinedione treatment increased FFA uptake and oxidation into cultured human skeletal muscle cells in concert with upregulation of FAT/CD36 expression. Increased FFA uptake and oxidation may contribute to lower circulating FFA levels and reduced insulin resistance in skeletal muscle of individuals with type 2 diabetes following thiazolidinedione treatment.
    Type of Medium: Online Resource
    ISSN: 0193-1849 , 1522-1555
    URL: Article
    DOI: 10.1152/ajpendo.00491.2001
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2003
    detail.hit.zdb_id: 1477331-4
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  • 6
    Online Resource
    Online Resource
    Excessive secretion of IL-8 by skeletal muscle in type 2 diabetes impairs tube growth: potential role of PI3K and the Tie2 receptor
    American Physiological Society ; 2015
    In:  American Journal of Physiology-Endocrinology and Metabolism Vol. 309, No. 1 ( 2015-07-01), p. E22-E34
    Details
    In: American Journal of Physiology-Endocrinology and Metabolism, American Physiological Society, Vol. 309, No. 1 ( 2015-07-01), p. E22-E34
    Abstract: Reduced capillary density is a feature of skeletal muscle (SkM) in type 2 diabetes (T2D), which is associated with multiple metabolic and functional abnormalities. SkM has been identified as a secretory tissue, releasing myokines that regulate multiple processes, including vascularization. We sought to determine how myokines secreted from T2D myotubes might influence SkM angiogenesis. Conditioned media (CM) were generated by myotubes from T2D and nondiabetic (ND) subjects. Primary human endothelial cells (HUVEC) and SkM explants were exposed to CM or recombinant myokines, and tube number or capillary outgrowth was determined as well as measurement of protein expression and phosphorylation. CM from ND myotubes stimulated tube formation of HUVEC to a greater extent than T2D myotubes (T2D-CM = 100%, ND-CM = 288 ± 90% after 48 h, P 〈 0.05). The effects of T2D myotube CM were mediated by IL-8, not IL-15 or GROα, and were due not to cell damage but rather through regulating tube production and maintenance (response to T2D-IL-8 = 100%, response to ND-IL-8 = 263 ± 46% after 48 h, P 〈 0.05). A similar effect was seen in SkM explants with exposure to IL-8. The dose-dependent effect of IL-8 on tube formation was also observable in the PI3K and FAK signaling pathways and mediated at least in part by PI3K, leading to regulation of Tie2 expression. These results suggest that elevated levels of IL-8 secreted from T2D myotubes create a muscle microenvironment that supports reduced capillarization in T2D. Impaired vascularization of SkM limits the availability of substrates, including glucose and contributes to the T2D phenotype.
    Type of Medium: Online Resource
    ISSN: 0193-1849 , 1522-1555
    URL: Article
    DOI: 10.1152/ajpendo.00513.2014
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2015
    detail.hit.zdb_id: 1477331-4
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  • 7
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    Online Resource
    Troglitazone but not Metformin Restores Insulin-Stimulated Phosphoinositide 3-Kinase Activity and Increases p110β Protein Levels in Skeletal Muscle of Type 2 Diabetic Subjects
    American Diabetes Association ; 2002
    In:  Diabetes Vol. 51, No. 2 ( 2002-02-01), p. 443-448
    Details
    In: Diabetes, American Diabetes Association, Vol. 51, No. 2 ( 2002-02-01), p. 443-448
    Abstract: Insulin stimulation of phosphatidylinositol (PI) 3-kinase activity is defective in skeletal muscle of type 2 diabetic individuals. We studied the impact of antidiabetic therapy on this defect in type 2 diabetic subjects who failed glyburide treatment by the addition of troglitazone (600 mg/day) or metformin (2,550 mg/day) therapy for 3–4 months. Improvement in glycemic control was similar for the two groups, as indicated by changes in fasting glucose and HbA1c levels. Insulin action on whole-body glucose disposal rate (GDR) was determined before and after treatment using the hyperinsulinemic (300 mU · m−2 · min−1) euglycemic (5.0–5.5 mmol/l) clamp technique. Needle biopsies of vastus lateralis muscle were obtained before and after each 3-h insulin infusion. Troglitazone treatment resulted in a 35 ± 9% improvement in GDR (P & lt; 0.01), which was greater than (P & lt; 0.05) the 22 ± 13% increase (P & lt; 0.05) after metformin treatment. Neither treatment had any effect on basal insulin receptor substrate-1 (IRS-1)-associated PI 3-kinase activity in muscle. However, insulin stimulation of PI 3-kinase activity was augmented nearly threefold after troglitazone treatment (from 67 ± 22% stimulation over basal pre-treatment to 211 ± 62% post-treatment, P & lt; 0.05), whereas metformin had no effect. The troglitazone effect on PI 3-kinase activity was associated with a 46 ± 22% increase (P & lt; 0.05) in the amount of the p110β catalytic subunit of PI 3-kinase. Insulin-stimulated Akt activity also increased after troglitazone treatment (from 32 ± 8 to 107 ± 32% stimulation, P & lt; 0.05) but was unchanged after metformin therapy. Protein expression of other key insulin signaling molecules (IRS-1, the p85 subunit of PI 3-kinase, and Akt) was unaltered after either treatment. We conclude that the mechanism for the insulin-sensitizing effect of troglitazone, but not metformin, involves enhanced PI 3-kinase pathway activation in skeletal muscle of obese type 2 diabetic subjects.
    Type of Medium: Online Resource
    ISSN: 0012-1797 , 1939-327X
    URL: Article
    DOI: 10.2337/diabetes.51.2.443
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2002
    detail.hit.zdb_id: 1501252-9
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  • 8
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    Online Resource
    Modulation of Circulating and Adipose Tissue Adiponectin Levels by Antidiabetic Therapy
    American Diabetes Association ; 2003
    In:  Diabetes Vol. 52, No. 3 ( 2003-03-01), p. 667-674
    Details
    In: Diabetes, American Diabetes Association, Vol. 52, No. 3 ( 2003-03-01), p. 667-674
    Abstract: The relationship between insulin action and control of the adipocyte-derived factor adiponectin was studied in age- and weight-matched obese individuals with type 2 diabetes failing sulfonylurea therapy. After initial metabolic characterization, subjects were randomized to troglitazone or metformin treatment groups; all subjects received glyburide (10 mg BID) as well. Treatment was continued for 3 months. The extent of glycemic control after treatment was similar in both groups. However, the increase in maximal insulin-stimulated glucose disposal rate was greater following troglitazone therapy (+44%) compared with metformin treatment (+20%). Troglitazone treatment increased serum adiponectin levels nearly threefold. There was no change in serum adiponectin with metformin treatment. A positive correlation was found between increases in whole-body glucose disposal rates and serum adiponectin levels after troglitazone; no such relationship was seen with metformin. The adiponectin protein content of subcutaneous abdominal adipocytes was increased following troglitazone treatment and unchanged after metformin. Adiponectin release from adipocytes was also augmented with troglitazone treatment. Adiponectin was present in adipocytes and plasma in several multimeric forms; a trimer was the major form secreted from adipocytes. These results indicate that increases in adiponectin content and secretion are associated with improved insulin action but are not directly related to glycemic control. Modulation of adipocyte function, including upregulation of adiponectin synthesis and secretion, may be an important mechanism by which thiazolidinediones influence insulin action.
    Type of Medium: Online Resource
    ISSN: 0012-1797 , 1939-327X
    URL: Article
    DOI: 10.2337/diabetes.52.3.667
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2003
    detail.hit.zdb_id: 1501252-9
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  • 9
    Online Resource
    Online Resource
    Regulation of Glucose Transport and Insulin Signaling by Troglitazone or Metformin in Adipose Tissue of Type 2 Diabetic Subjects
    American Diabetes Association ; 2002
    In:  Diabetes Vol. 51, No. 1 ( 2002-01-01), p. 30-36
    Details
    In: Diabetes, American Diabetes Association, Vol. 51, No. 1 ( 2002-01-01), p. 30-36
    Abstract: Type 2 diabetic subjects failing glyburide therapy were randomized to receive additional therapy with either metformin (2,550 mg/day) or troglitazone (600 mg/day) for 3–4 months. Biopsies of subcutaneous abdominal adipose tissue were obtained before and after therapy. Glycemic control was similar with both treatments. Metformin treatment increased insulin-stimulated whole-body glucose disposal rates by 20% (P & lt; 0.05); the response to troglitazone was greater (44% increase, P & lt; 0.01 vs. baseline, P & lt; 0.05 vs. metformin). Troglitazone-treated subjects displayed a tendency toward weight gain (5 ± 2 kg, P & lt; 0.05), increased adipocyte size, and increased serum leptin levels. Metformin-treated subjects were weight-stable, with unchanged leptin levels and reduced adipocyte size (to 84 ± 4% of control, P & lt; 0.005). Glucose transport in isolated adipocytes from metformin-treated subjects was unaltered from pretreatment. Glucose transport in both the absence (321 ± 134% of pre-Rx, P & lt; 0.05) and presence of insulin (418 ± 161%, P & lt; 0.05) was elevated after troglitazone treatment. Metformin treatment had no effect on adipocyte content of GLUT1 or GLUT4 proteins. After troglitazone treatment, GLUT4 protein expression was increased twofold (202 ± 42%, P & lt; 0.05). Insulin-stimulated serine phosphorylation of Akt was augmented after troglitazone (170 ± 34% of pre-Rx response, P & lt; 0.05) treatment and unchanged by metformin. We conclude that the ability of troglitazone to upregulate adipocyte glucose transport, GLUT4 expression, and insulin signaling can contribute to its greater effect on whole-body glucose disposal.
    Type of Medium: Online Resource
    ISSN: 0012-1797 , 1939-327X
    URL: Article
    DOI: 10.2337/diabetes.51.1.30
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2002
    detail.hit.zdb_id: 1501252-9
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  • 10
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    Online Resource
    Inhibition of Glycogen Synthase Kinase 3 Improves Insulin Action and Glucose Metabolism in Human Skeletal Muscle
    American Diabetes Association ; 2002
    In:  Diabetes Vol. 51, No. 7 ( 2002-07-01), p. 2190-2198
    Details
    In: Diabetes, American Diabetes Association, Vol. 51, No. 7 ( 2002-07-01), p. 2190-2198
    Abstract: Glycogen synthase kinase (GSK)-3 has been implicated in the regulation of multiple cellular physiological processes in skeletal muscle. Selective cell-permeable reversible inhibitors (INHs) of GSK-3 (CT98014 and CHIR98023 [Chiron, Emeryville, CA] and LiCl) were used to evaluate the role of GSK-3 in controlling glucose metabolism. Acute treatment (30 min) of cultured human skeletal muscle cells with either INH resulted in a dose-dependent activation of glycogen synthase (GS) with a maximally effective concentration of ∼2 μmol/l. The maximal acute effect of either INH on GS (103 ± 25% stimulation over basal) was greater than the maximal insulin response (48 ± 9%, P & lt; 0.05 vs. INH); LiCl was as effective as insulin. The GSK-3 inhibitor effect, like that of insulin, was on the activation state (fractional velocity [FV]) of GS. Cotreatment of muscle cells with submaximal doses of INH and insulin resulted in an additive effect on GS FV (103 ± 10% stimulation, P & lt; 0.05 vs. either agent alone). Glucose incorporation into glycogen was also acutely stimulated by INH. While prolonged (6–24 h) insulin exposure led to desensitization of GS, INH continued to activate GS FV for at least 24 h. Insulin and LiCl acutely activated glucose uptake, whereas INH stimulation of glucose uptake required more prolonged exposure, starting at 6 h and continuing to 24 h. Chronic (4-day) treatment with INH increased both basal (154 ± 32% of control) and insulin-stimulated (219 ± 74%) glucose uptake. Upregulation of uptake activity occurred without any change in total cellular GLUT1 or GLUT4 protein content. Yet the same chronic treatment resulted in a 65 ± 6% decrease in GSK-3 protein and a parallel decrease (61 ± 11%) in GSK-3 total activity. Together with the INH-induced increase in insulin-stimulated glucose uptake, there was an ∼3.5-fold increase (P & lt; 0.05) in insulin receptor substrate (IRS)-1 protein abundance. Despite upregulation of IRS-1, maximal insulin stimulation of Akt phosphorylation was unaltered by INH treatment. The results suggest that selective inhibition of GSK-3 has an impact on both GS and glucose uptake, including effects on insulin action, using mechanisms that differ from and are additive to those of insulin.
    Type of Medium: Online Resource
    ISSN: 0012-1797 , 1939-327X
    URL: Article
    DOI: 10.2337/diabetes.51.7.2190
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2002
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