Diabetes
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This study evaluates whether diffusion tensor imaging magnetic resonance neurography (DTI-MRN), T2 relaxation time, and proton spin density can detect and grade neuropathic abnormalities in patients with type 1 diabetes. Patients with type 1 diabetes (n = 49) were included-11 with severe polyneuropathy (sDPN), 13 with mild polyneuropathy (mDPN), and 25 without polyneuropathy (nDPN)-along with 30 healthy control subjects (HCs). Clinical examinations, nerve conduction studies, and vibratory perception thresholds determined the presence and severity of DPN. ⋯ Quantitative group differences in proton spin density were also significant, but less pronounced than those for DTI-MRN. In conclusion, DTI-MRN enables detection in peripheral nerves of abnormalities related to DPN, more so than proton spin density or T2 relaxation time. These abnormalities are likely to reflect pathology in sciatic and tibial nerve fibers.
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Hepatic FAM3A expression is repressed under obese conditions, but the underlying mechanism remains unknown. This study determined the role and mechanism of miR-423-5p in hepatic glucose and lipid metabolism by repressing FAM3A expression. miR-423-5p expression was increased in the livers of obese diabetic mice and in patients with nonalcoholic fatty liver disease (NAFLD) with decreased FAM3A expression. miR-423-5p directly targeted FAM3A mRNA to repress its expression and the FAM3A-ATP-Akt pathway in cultured hepatocytes. Hepatic miR-423-5p inhibition suppressed gluconeogenesis and improved insulin resistance, hyperglycemia, and fatty liver in obese diabetic mice. ⋯ The miR-423 precursor gene was further shown to be a target gene of NFE2, which induced miR-423-5p expression to repress the FAM3A-ATP-Akt pathway in cultured hepatocytes. Hepatic NFE2 overexpression upregulated miR-423-5p to repress the FAM3A-ATP-Akt pathway, promoting gluconeogenesis and lipid deposition and causing hyperglycemia in normal mice. In conclusion, under the obese condition, activation of the hepatic NFE2/miR-423-5p axis plays important roles in the progression of type 2 diabetes and NAFLD by repressing the FAM3A-ATP-Akt signaling pathway.