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Changes in Pain Threshold in the Early Stages of Type I Diabetes
Author(s) -
YBARBO KAI,
GROTLE ANNKATRIN,
HUO YU,
STONE AUDREY
Publication year - 2019
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2019.33.1_supplement.lb633
Subject(s) - medicine , allodynia , threshold of pain , peripheral neuropathy , hyperalgesia , type 1 diabetes , hypoalgesia , diabetes mellitus , stimulation , endocrinology , anesthesia , nociception , neuropathic pain , chronic pain , streptozotocin , receptor , psychiatry
Type 1 diabetes mellitus (T1DM) is a metabolic disease in which chronic hyperglycemia increases the risk of developing peripheral neuropathy. A common early symptom of peripheral neuropathy is mechanical allodynia, which is characterized as painful sensation to a normally non‐painful stimulus. However, whether the expression of mechanical allodynia changes with the progression of the disease is not fully understood. Therefore, the purpose of this study was to determine changes in pain threshold to mechanical stimulation during the early stages of T1DM. Adult male and female Sprague‐Dawley rats were given 3–4 sessions of acclimation to cereal and the von Frey testing cage and were not deprived of food at any time. Pain threshold was measured with von Frey monofilaments, which were applied to the L5 dermatome on the plantar surface of the rat's hindpaw until the filament bent. The lowest force that elicited a quick paw withdrawal was measured and averaged between the responses of both hindpaws. We defined mechanical allodynia as a significant reduction in force required to elicit paw withdrawal compared to baseline levels. Following baseline measurements of pain threshold, non‐fasted blood glucose level, and body weight, rats were injected with either streptozotocin (STZ; 50mg/kg i.p.), a known toxin that destroys pancreatic beta cells and induces T1DM, or citrate buffer (CTL), the vehicle control for STZ. One week and two weeks post injection, body weight, blood glucose level, and pain threshold were again measured. We found that pain threshold was significantly reduced (p<0.05) 2 weeks after STZ injection (before STZ: 88 ± 10 g, n=4; after STZ: 22 ± 10 g, n=4), but not 1 week after STZ injection (before STZ: 32 ± 15 g, n=7; after STZ: 12 ± 5 g, n=7) compared to baseline. No significant difference was seen in CTL rats 1 week after injection (before CTL: 56 ± 23 g, n=6; after CTL: 48 ± 14 g, n=6) compared to baseline. Body weight was significantly reduced (p<0.05) in STZ rats at 1 week (before STZ: 426 ± 42 g, n=7; after STZ: 377 ± 31 g, n=7) and 2 weeks (before STZ: 397 ± 8 g, n=4; after STZ: 300 ± 8 g, n=4) after injection, but did not change in CTL rats (before CTL: 436 ± 29 g, n=6; after CTL: 446 ± 29 g, n=6). These findings suggest that mechanical allodynia is present as early as 2 weeks following the destruction of insulin producing beta cells. This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .