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    insulin resistance tagged posts

    Cause of Inflammation in Diabetes identified

    November 2, 2016, Categories  Uncategorized

    Too much fat in the diet promotes insulin resistance by spurring chronic inflammation. In the image above, immune cells (shown in green) produce fatty acids that contribute to diabetes-related inflammation. Researchers at Washington University School of Medicine have developed a way to block production of fatty acids in these immune cells in mice and protect them from diet-induced diabetes. Credit: Semenkovich lab/ Washington University

    Too much fat in the diet promotes insulin resistance by spurring chronic inflammation. In the image above, immune cells (shown in green) produce fatty acids that contribute to diabetes-related inflammation. Researchers at Washington University School of Medicine have developed a way to block production of fatty acids in these immune cells in mice and protect them from diet-induced diabetes. Credit: Semenkovich lab/ Washington University

    Inflammation is one of the main reasons why people with diabetes experience heart attacks, strokes, kidney problems and other, related complications. Now, in a surprise finding, researchers at Washington University School of Medicine in St. Louis have identified a possible trigger of chronic inflammation...

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    Bright Light Alters Metabolism

    May 18, 2016, Categories  Biology/Biotechnology, Health/Medical

    Surfing internet before sleep. Scientists found bright light exposure increased insulin resistance compared to dim light exposure in both the morning and the evening. In the evening, bright light also caused higher peak glucose (blood sugar) levels. Credit: © Sergey Nivens / Fotolia

    Surfing internet before sleep. Scientists found bright light exposure increased insulin resistance compared to dim light exposure in both the morning and the evening. In the evening, bright light also caused higher peak glucose (blood sugar) levels. Credit: © Sergey Nivens / Fotolia

    Northwestern scientists found bright light exposure increased insulin resistance compared to dim light exposure in both the morning and the evening. In the evening, bright light also caused higher peak glucose (blood sugar) levels. Over time, the excess blood glucose could result in increased body fat, weight gain and a higher risk for diabetes. “These results provide further evidence that bright light exposure may influence metabolism,” said Prof. Kathryn Reid.

    Previous research by Northwestern scientists sho...

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    Why is Visceral Fat Worse than Subcutaneous Fat?

    April 26, 2016, Categories  Biology/Biotechnology, Health/Medical

    Model for the regulation of visceral fat ER stress in obesity.

    Model for the regulation of visceral fat ER stress in obesity. Induction of TRIP-Br2 and GATA3 during obesity via ER stress is critical for the visceral fat proinflammatory responses.

    Researchers have long-known that visceral fat (which wraps around the internal organs) is more dangerous than subcutaneous fat (under the skin). But how visceral fat contributes to insulin resistance and inflammation has remained unknown. A study points blame at a regulatory molecule in cells called TRIP-Br2 that is produced in response to overeating’s stress on the machinery cells use to produce proteins.

    In previous studies, in obese humans TRIP-Br2 was turned-up in visceral fat but not in subcutaneous fat...

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    New Links between Heart Hormones, Obesity, and Diabetes

    February 17, 2016, Categories  Biology/Biotechnology, Health/Medical

    Summary of NP action in the skeletal muscle in healthy individuals (A) and obese individuals with diabetes (B). NPs circulate in reduced concentrations in obese individuals with diabetes compared with the levels in healthy individuals. Furthermore, expression of NPRA, which binds NPs and activates intracellular signaling events, is reduced, while expression of NPRC, which clears NPs in tissues, is increased in obesity and T2D. In healthy individuals, generation of cGMP from guanosine triphosphate (GTP) by the guanylyl cyclase activity of NPRA activates a signaling pathway resulting in the phosphorylation (P) and activation of p38 mitogen-activated protein kinase (p38 MAPK) and the increased transcription of peroxisome proliferator–activated receptor coactivator γ-1α (PGC1α). This is associated with mitochondrial biogenesis and oxidation of lipids, including the lipotoxic diacylglycerols (DAGs) and ceramides. In obese individuals, NP signaling from NPRA is attenuated, predisposing to DAG and ceramide accumulation in the muscle and thus IR, characterized by inhibition of insulin signaling via Akt and impaired glucose disposal.

    Summary of NP action in the skeletal muscle in healthy individuals (A) and obese individuals with diabetes (B). NPs circulate in reduced concentrations in obese individuals with diabetes compared with the levels in healthy individuals. Furthermore, expression of NPRA, which binds NPs and activates intracellular signaling events, is reduced, while expression of NPRC, which clears NPs in tissues, is increased in obesity and T2D. In healthy individuals, generation of cGMP from guanosine triphosphate (GTP) by the guanylyl cyclase activity of NPRA activates a signaling pathway resulting in the phosphorylation (P) and activation of p38 mitogen-activated protein kinase (p38 MAPK) and the increased transcription of peroxisome proliferator–activated receptor coactivator γ-1α (PGC1α)...

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