High-Intensity Interval Training, Caloric Restriction, or Their Combination Have Beneficial Effects on Metabolically Acquired Peripheral Neuropathy.

Autor:	Eid SA; Department of Neurology, University of Michigan, Ann Arbor, MI., Elzinga SE; Department of Neurology, University of Michigan, Ann Arbor, MI., Kim B; Department of Neurology, University of Michigan, Ann Arbor, MI., Rumora AE; Department of Neurology, University of Michigan, Ann Arbor, MI.; Department of Neurology, Columbia University, New York, NY., Hayes JM; Department of Neurology, University of Michigan, Ann Arbor, MI., Carter A; Department of Neurology, University of Michigan, Ann Arbor, MI., Pacut C; Department of Neurology, University of Michigan, Ann Arbor, MI., Allouch AM; Department of Neurology, University of Michigan, Ann Arbor, MI., Koubek EJ; Department of Neurology, University of Michigan, Ann Arbor, MI., Feldman EL; Department of Neurology, University of Michigan, Ann Arbor, MI.
Jazyk:	angličtina
Zdroj:	Diabetes [Diabetes] 2024 Nov 01; Vol. 73 (11), pp. 1895-1907.
DOI:	10.2337/db23-0997
Abstrakt:	Peripheral neuropathy (PN) is a prevalent and debilitating complication of obesity, prediabetes, and type 2 diabetes, which remains poorly understood and lacks disease-modifying therapies. Fortunately, diet and/or exercise have emerged as effective treatment strategies for PN. Here, we examined the impact of caloric restriction (CR) and high-intensity interval training (HIIT) interventions, alone or combined (HIIT-CR), on metabolic and PN outcomes in high-fat diet (HFD) mice. HFD feeding alone resulted in obesity, impaired glucose tolerance, and PN. Peripheral nerves isolated from these mice also developed insulin resistance (IR). CR and HIIT-CR, but not HIIT alone, improved HFD-induced metabolic dysfunction. However, all interventions improved PN to similar extents. When examining the underlying neuroprotective mechanisms in whole nerves, we found that CR and HIIT-CR activate the fuel-sensing enzyme AMPK. We then performed complimentary in vitro work in Schwann cells, the glia of peripheral nerves. Treating primary Schwann cells with the saturated fatty acid palmitate to mimic prediabetic conditions caused IR, which was reversed by the AMPK activator, AICAR. Together, these results enhance our understanding of PN pathogenesis, the differential mechanisms by which diet and exercise may improve PN, and Schwann cell-specific contributions to nerve insulin signaling and PN progression. (© 2024 by the American Diabetes Association.)
Databáze:	MEDLINE
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