Publications by authors named "S E Elzinga"

Article Synopsis
  • Peripheral neuropathy (PN) is a common yet poorly understood complication of obesity and diabetes, with current treatments lacking effectiveness.
  • Research showed that caloric restriction (CR) and high-intensity interval training (HIIT), especially when combined, can improve metabolic issues caused by a high-fat diet in mice, while all methods effectively alleviated PN symptoms.
  • The studies revealed that CR and HIIT-CR activate the enzyme AMPK, which plays a key role in neuroprotection, and that enhancing insulin signaling in Schwann cells helps reverse insulin resistance linked to PN.
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Peripheral neuropathy (PN) is a severe and frequent complication of obesity, prediabetes, and type 2 diabetes characterized by progressive distal-to-proximal peripheral nerve degeneration. However, a comprehensive understanding of the mechanisms underlying PN, and whether these mechanisms change during PN progression, is currently lacking. Here, gene expression data were obtained from distal (sciatic nerve; SCN) and proximal (dorsal root ganglia; DRG) injury sites of a high-fat diet (HFD)-induced mouse model of obesity/prediabetes at early and late disease stages.

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Pituitary pars intermedia dysfunction (PPID) is an age-related neurodegenerative disorder, affecting >20 % of older horses. There is a need for improved endocrine tests for early disease detection, and the thyrotropin-releasing hormone (TRH) stimulation test has been recommended for diagnosis of early or mild cases. However, it is currently not recommended for year-round use due to marked seasonal variability.

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Diabetic kidney disease (DKD) and diabetic peripheral neuropathy (DPN) are common complications of type 1 (T1D) and type 2 (T2D) diabetes. However, the mechanisms underlying pathogenesis of these complications are unclear. In this study, we optimized a streptozotocin-induced db/+ murine model of T1D and compared it to our established db/db T2D mouse model of the same C57BLKS/J background.

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