J Pediatr Gastroenterol Nutr
December 2023
Objectives: Insulin resistance (IR) affects children and adolescents with obesity and early diagnosis is crucial to prevent long-term consequences. Our aim was to identify predictors of IR and develop a multivariate model to accurately predict IR.
Methods: We conducted a cross-sectional analysis of demographical, clinical, and biochemical data from a cohort of patients attending a specialized Paediatric Nutrition Unit in Portugal over a 20-year period.
Painful diabetic neuropathy (PDN) induces neuronal hyperactivity at the spinal cord and periaqueductal gray (PAG), a key area in descending nociceptive modulation. Since the PAG uses relay stations at serotoninergic and noradrenergic brainstem areas, we determined the serotonin and noradrenaline levels at the spinal cord of streptozotocin-diabetic rats and at those brainstem areas (serotoninergic rostroventromedial medulla and noradrenergic A(5) and A(7) cell groups). Since, during diabetes, the levels of insulin growth factor 1 (IGF1) decrease, reducing its neurotrophic effect in the brain, we also studied the effects of IGF1 treatment.
View Article and Find Full Text PDFPainful diabetic neuropathy may be due to impairments in descending modulation of nociceptive transmission at the spinal cord. In the present study, streptozotocin diabetic rats (STZ rats) with neuropathic symptoms (mechanical hypersensitivity) were used to perform a time-course evaluation of neuronal activity at the spinal dorsal horn and at the periaqueductal grey matter (PAG), a major brainstem area of pain modulation. The expression of Fos protein, a marker of nociceptive activation, progressively increased at the spinal dorsal horn at 4 and 10 weeks.
View Article and Find Full Text PDFPainful diabetic neuropathy is associated to hyperexcitability and spontaneous hyperactivity of spinal cord neurons. The underlying pathophysiological mechanisms are not clear. Increases in excitatory neurotransmission at the spinal cord, involving glutamate and SP, seem to account for the abnormal neuronal activity, but inhibitory influences were never evaluated.
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