Key result
Normoglycemic obesity shows comparable peripheral neuropathy prevalence to long-duration type 1 diabetes.
Why the study?
Peripheral neuropathy is reported in obesity even without hyperglycaemia, prompting a comparison of its prevalence and phenotype between individuals with obesity and long-duration type 1 diabetes.
Cross-Sectional (n=130)
No
The prevalence and phenotype of peripheral neuropathy are comparable between normoglycaemic people with obesity and long-duration type 1 diabetes, suggesting obesity-related risk factors contribute significantly to neuropathy.
This is the authors' abstract. We don't add key points for this paper.
Peripheral neuropathy is reported in obesity even in the absence of hyperglycaemia. To compare the prevalence and characterise the phenotype of peripheral neuropathy in people living with obesity (OB) and long-duration type 1 diabetes (T1D). We performed a prospective cross-sectional study of 130 participants including healthy volunteers (HV) (n = 28), people with T1D (n = 51), and OB (BMI 30–50 kg/m2) (n = 51). Participants underwent assessment of neuropathic symptoms (Neuropathy Symptom Profile, NSP), neurological deficits (Neuropathy Disability Score, NDS), vibration perception threshold (VPT) and evaluation of sural nerve conduction velocity and amplitude. Peripheral neuropathy was present in 43.1% of people with T1D (age 49.9 ± 12.9 years; duration of diabetes 23.4 ± 13.5 years) and 33.3% of OB (age 48.2 ± 10.8 years). VPT for high risk of neuropathic foot ulceration (VPT ≥ 25 V) was present in 31.4% of T1D and 19.6% of OB. Participants living with OB were heavier (BMI 42.9 ± 3.5 kg/m2) and had greater centripetal adiposity with an increased body fat percentage (FM%) (P < 0.001) and waist circumference (WC) (P < 0.001) compared to T1D. The OB group had a higher NDS (P < 0.001), VAS for pain (P < 0.001), NSP (P < 0.001), VPT (P < 0.001) and reduced sural nerve conduction velocity (P < 0.001) and amplitude (P < 0.001) compared to HV, but these parameters were comparable in T1D. VPT was positively associated with increased WC (P = 0.011), FM% (P = 0.001) and HbA1c (P < 0.001) after adjusting for age (R2 = 0.547). Subgroup analysis of respiratory quotient (RQ) measured in the OB group did not correlate with VPT (P = 0.788), nerve conduction velocity (P = 0.743) or amplitude (P = 0.677). The characteristics of peripheral neuropathy were comparable between normoglycaemic people living with obesity and people with long-duration T1D, suggesting that metabolic factors linked to obesity play a pivotal role in the development of peripheral neuropathy. Further studies are needed to investigate the mechanistic link between visceral adiposity and neuropathy.
Answers are grounded in this paper and cite their sources.
Suggests obesity-related neuropathy may warrant clinical attention akin to T1D; hypothesis-generating and leaves open causal mechanisms and interventions.
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Lim et al. (2022) conducted a cross-sectional in Peripheral neuropathy (n=130). Obesity vs. Type 1 Diabetes was evaluated on Prevalence of peripheral neuropathy (Toronto consensus criteria). The prevalence of peripheral neuropathy was comparable between normoglycaemic people living with obesity (33.3%) and people with long-duration type 1 diabetes (43.1%).
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