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hyperalgesia/obesidad
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Behavioral evidence of thermal hyperalgesia in non-obese diabetic mice with and without insulin-dependent diabetes.
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The non-obese diabetic (NOD) mouse, a model of Type 1 diabetes in humans, has proven useful for the study of genetic, immunologic and epidemiologic aspects of inherited diabetes. Behavioral evidence of hyperalgesia may also be present in the NOD mouse but has not been described. This study examined
Treatment effects on pain catastrophizing and cutaneous allodynia symptoms in women with migraine and overweight/obesity
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Objective: Pain catastrophizing and cutaneous allodynia represent two risk factors for greater headache-related disability. Yet, there is limited knowledge of the extent to which these risk factors are modifiable and whether
Hyperalgesia in non-obese diabetic (NOD) mice: a role for the inducible bradykinin B1 receptor.
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Most studies performed to investigate the role of the inducible bradykinin B(1) receptor in the pathology and complications of type 1 diabetes have been carried out using the model of streptozotocin (STZ)-induced diabetes. The model of spontaneous autoimmune diabetes in non-obese diabetic (NOD) mice
Ursolic acid prevents augmented peripheral inflammation and inflammatory hyperalgesia in high-fat diet-induced obese rats by restoring downregulated spinal PPARα.
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Obesity is a risk factor for several pain syndromes and is associated with increased pain sensitivity. Evidence suggests that obesity causes the downregulation of peroxisome proliferator‑activated receptor (PPAR)α in the spinal cord, contributing to augmented peripheral edema and inflammatory
Liver X Receptors Protect Dorsal Root Ganglia from Obesity-Induced Endoplasmic Reticulum Stress and Mechanical Allodynia.
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Obesity is associated with many complications, including type 2 diabetes and painful neuropathy. There is no cure or prevention for obesity-induced pain, and the neurobiology underlying the onset of the disease is still obscure. In this study, we observe that western diet (WD)-fed mice developed
Down-regulation of PPARα in the spinal cord contributes to augmented peripheral inflammation and inflammatory hyperalgesia in diet-induced obese rats.
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Obesity is associated with augmented peripheral inflammation and pain sensitivity in response to inflammatory stimulation, but the underlying mechanisms remain unclear. Emerging evidence has shown that activation of peroxisome proliferator-activated receptor-α (PPARα) in the central nervous system
Increased central and peripheral inflammation and inflammatory hyperalgesia in Zucker rat model of leptin receptor deficiency and genetic obesity.
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This study investigated whether sensitivity to nociceptive stimuli is altered in obese rats using established models of inflammatory pain, and using real-time PCR, profiled alterations in expression of key adipokine and inflammatory mediator mRNA (adiponectin, tumor necrosis factor-α,
Modulation of diet-induced mechanical allodynia by metabolic parameters and inflammation.
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Dietary-associated diseases have increased tremendously in our current population, yet key molecular changes associated with high-fat diets that cause clinical pre-diabetes, obesity, hyperglycemia, and peripheral neuropathy remain unclear. This study examines molecular and metabolic aspects altered
Neurophysiological features of the nociceptive trigeminal pathway in abdominally obese migraineurs
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Objective: The aim of this study were to assess clinical (cutaneous allodynia) and neurophysiological (R2 nBR component) markers of the nociceptive trigeminal-cervical pathway sensitization in the abdominally obese patients with episodic
Ecological momentary assessment of the relationship between headache pain intensity and pain interference in women with migraine and obesity.
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Background While pain intensity during migraine headache attacks is known to be a determinant of interference with daily activities, no study has evaluated: (a) the pain intensity-interference association in real-time on a per-headache basis, (b) multiple interference domains, and (c) factors that
CXCL13/CXCR5 signaling contributes to diabetes-induced tactile allodynia via activating pERK, pSTAT3, pAKT pathways and pro-inflammatory cytokines production in the spinal cord of male mice.
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Painful diabetic neuropathy (PDN) is a severely debilitating chronic pain syndrome. Spinal chemokine CXCL13 and its receptor CXCR5 were recently demonstrated to play a pivotal role in the pathogenesis of chronic pain induced by peripheral tissue inflammation or nerve injury. In this study we
Intensity-dependent effects of aerobic training on pressure pain threshold in overweight men: A randomized trial.
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OBJECTIVE
To investigate the chronic and acute effects of high-intensity interval training (HIIT) and moderate-intensity continuous training (MICT) on pressure pain thresholds (PPT) in overweight men.
METHODS
Twenty-eight participants performed stationary cycling exercise three times per week for 6
Effect of tempol on peripheral neuropathy in diet-induced obese and high-fat fed/low-dose streptozotocin-treated C57Bl6/J mice.
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In this study, we sought to determine the efficacy of tempol on multiple neuropathic endpoints in a diet-induced obese mouse, a model of pre-diabetes, and a high-fat fed low-dose streptozotocin treated mouse, a model of type 2 diabetes. Tempol (4-hydroxy-2,2,6,6-tetramethylpiperdine -1-oxyl) is a
Systemic administration of 5-HT(2C) receptor agonists attenuates muscular hyperalgesia in reserpine-induced myalgia model.
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Fibromyalgia is a prevalent musculoskeletal disorder characterized by chronic widespread pain that significantly reduces quality of life in patients. Due to the lack of consistently effective treatment, the development of improved therapies for treating fibromyalgia is necessary. As dysfunction of
Pain worsening with physical activity during migraine attacks in women with overweight/obesity: A prospective evaluation of frequency, consistency, and correlates.
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Background Migraine is a neurological disease involving recurrent attacks of moderate-to-severe and disabling head pain. Worsening of pain with routine physical activity during attacks is a principal migraine symptom; however, the frequency, individual consistency, and correlates of this symptom are
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