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Showing 1–15 of 15 results
Advanced filters: Author: Rexford S. Ahima Clear advanced filters
  • Obesity accelerates the aging of adipose tissue, a process only now beginning to come to light at the molecular level. Experiments in mice suggest that obesity increases the formation of reactive oxygen species in fat cells, shortens telomeres—and ultimately results in activation of the p53 tumor suppressor, inflammation and the promotion of insulin resistance (pages 1082–1087).

    • Rexford S. Ahima
    News & Views
    Nature Medicine
    Volume: 15, P: 996-997
  • This paper shows that specific genetic disruption of the Ncor–HdaC3 interaction in mice causes aberrant regulation of clock genes and results in abnormal circadian behaviour. These mice are also leaner and more insulin sensitive due to increased energy expenditure. Loss of a functional Ncor–HdaC3 complex in vivo changes the oscillatory patterns of several metabolic genes, demonstrating that circadian regulation of metabolism is critical for normal energy balance.

    • Theresa Alenghat
    • Katherine Meyers
    • Mitchell A. Lazar
    Research
    Nature
    Volume: 456, P: 997-1000
  • Obesity is commonly associated with leptin resistance. Inhibition of HDAC6 in adipose tissue of mice with diet-induced obesity produces a protein factor that augments leptin’s ability to reduce feeding and body weight, and improve glucose tolerance. HDAC6 inhibition acts as a novel treatment for obesity by ameliorating leptin resistance.

    • Rexford S. Ahima
    News & Views
    Nature Metabolism
    Volume: 4, P: 11-12
  • Ciliary neurotrophic factor (CNTF) enhances fatty-acid oxidation in muscle and reduces insulin resistance in obese, diabetic mice. Because skeletal muscle is the major site of insulin-mediated glucose uptake, this action of CNTF could benefit individuals with diabetes (pages 541–548).

    • Rexford S Ahima
    News & Views
    Nature Medicine
    Volume: 12, P: 511-512
  • The insulin signaling pathway regulating glucose homeostasis that has been well accepted is insulin-to-insulin receptor-to-IRS proteins-to-PI3K-to-Akt-to-Foxo1—a pathway that does not respond properly in states of insulin resistance, including type 2 diabetes. In a new study from Morris Birnbaum and colleagues, an alternative insulin signaling pathway has been uncovered, as mice with liver-specific deletion of Akt and Foxo1 still respond normally to nutritional cues and properly regulate glucose metabolism. Although the exact nature of this alternative pathway needs to be identified, the results should open many new avenues of exploration in the field of type 2 diabetes.

    • Mingjian Lu
    • Min Wan
    • Morris J Birnbaum
    Research
    Nature Medicine
    Volume: 18, P: 388-395
  • It is believed that lipid accumulation in the liver, or fatty liver disease, contributes to insulin resistance in this organ and, thus, poorly controlled gluconeogenesis and hyperglycemia during type 2 diabetes. Mitch Lazar and colleagues now show that deletion of the chromatin modifier Hdac3 in mice results in increased fatty liver disease but improved hepatic insulin sensitivity because metabolic flux in the liver is increased toward lipid synthesis and storage and away from gluconeogenesis.

    • Zheng Sun
    • Russell A Miller
    • Mitchell A Lazar
    Research
    Nature Medicine
    Volume: 18, P: 934-942
  • Alzheimer disease (AD) and related dementias share numerous mechanistic and epidemiological similarities with type 2 diabetes mellitus (T2DM). However, whether these associations result from synergistic interactions between the disorders is unclear. This Review summarizes our current knowledge regarding insulin signalling and resistance in the brain and discusses current evidence concerning neurological impairment in T2DM and insulin resistance in AD.

    • Steven E. Arnold
    • Zoe Arvanitakis
    • David M. Nathan
    Reviews
    Nature Reviews Neurology
    Volume: 14, P: 168-181