ArticleBMC obesity2016
Somatic neural alterations in non-diabetic obesity: a cross-sectional study.
Article in BMC obesity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
7 citing papers in PubMed, 16 citations in OpenAlex.
- Assessment of Urethral Elasticity by Shear Wave Elastography: A Novel Parameter Bridging a Gap Between Hypermobility and ISD in Female Stress Urinary Incontinence.Bioengineering (Basel, Switzerland) · 2025Article
- Somatosensory innervation of adipose tissues.Physiology & behavior · 2023Review
- Diagnosis and treatment of meralgia paresthetica between 2005 and 2018: a national cohort study.Neurosurgical review · 2023Article
- The role of abnormalities of lipoproteins and HDL functionality in small fibre dysfunction in people with severe obesity.Scientific reports · 2021Article
- Early disruption of nerve mitochondrial and myelin lipid homeostasis in obesity-induced diabetes.JCI insight · 2020Article
- Molecular pathways linking adipose innervation to insulin action in obesity and diabetes mellitus.Nature reviews. Endocrinology · 2019Review
- Obesity and Stress Urinary Incontinence: Impact on Pathophysiology and Treatment.Current urology reports · 2018Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundReports on alterations in somatic neural functions due to non-diabetic obesity, a major risk factor for diabetes, are few and still a matter of debate. Nevertheless, to our knowledge, reports lack any comments on the type of somatic nerve fibers affected in non-diabetic obesity. Therefore, this study aimed to find out the alteration in somatic neural functions in non-diabetic obese persons if any.
methodsThe study was conducted on 30 adult non-diabetic obese persons (mean age 32.07 ± 7.25 years) with BMI > 30 Kg/m
resultsIn comparison to normal weight persons, obese had lower compound muscle action potential (CMAP) amplitudes of right median [9.09(7.62-10.20) Vs 10.75(8.71-12.2) mV,
conclusionThis study documents subclinical peripheral nerve damage in non-diabetic obese with abnormal NCS parameters; shorter amplitudes and prolonged CMAP and SNAP durations. The reduced amplitudes of mixed and sensory nerves might be due to decreased axonal number stimulation or actual decrease in number of axonal fibers, or defect at NMJ in non-diabetic obese. Prolonged durations but normal onset latencies and conduction velocities strongly suggest involvement of slow conducting fibers.
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