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Somatic neural alterations in non-diabetic obesity: a cross-sectional study

View Article: PubMed Central - PubMed

ABSTRACT

Background: Reports 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.

Methods: The study was conducted on 30 adult non-diabetic obese persons (mean age 32.07 ± 7.25 years) with BMI > 30 Kg/m2 (mean BMI 30.02 ± 2.89 Kg/m2) and 29 age- and sex-matched normal weight controls (mean age 30.48 ± 8.01 years) with BMI: 18–24Kg/m2 (mean BMI 21.87 ± 2.40 Kg/m2). Nerve conduction study (NCS) variables of median, tibial and sural nerves were assessed in each subject using standard protocol. The data were compared by Mann Whitney ‘U’ test.

Results: In 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, p = 0.025] and bilateral tibial nerves [Right: 8.5(7.04–11.18) Vs 12.1(10.55–15) mV, p < 0.001 and left 9.08(6.58–11.65) Vs 13.05(10.2–15.6) mV, p = 0.002]. Furthermore, obese persons had prolonged CMAP durations of right and left median [10.5(9.62–12) Vs 10(8.4–10.3) ms, p = 0.02 and 10.85(10–11.88) Vs 10(9–10.57) ms, p = 0.019] and right tibial [10(9–11) 8.5(7.92–10) ms, p = 0.032] nerves. Sensory NCS (sural nerve) also showed diminished sensory nerve action potential (SNAP) amplitude [16(12.08–18.21) vs 22.8(18.3–31.08) μV, p < 0.001] and prolonged duration. However, onset latencies and conduction velocities for all nerves were comparable between the groups.

Conclusion: This 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.

No MeSH data available.


Representative trace of tibial distal and proximal compound muscle action potential
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Fig1: Representative trace of tibial distal and proximal compound muscle action potential

Mentions: Once a recording was made, the trace was stored for later analysis and the stimulating electrode was moved proximally to the second site. The distance between stimulating electrodes at proximal and distal sites was measured with a measuring tape and was fed into the machine for nerve conduction velocity calculation. For each stimulation site, onset latency was measured in milliseconds from the stimulus artefact to the first deflection of CMAP whereas peak latency was measured at the midpoint of the first negative peak. CMAP amplitude was measured from baseline to the negative peak (base to peak) and duration of CMAP was measured from the onset to the final return of waveform to the baseline (Fig. 1). For recording F-response or the late response, the stimulator was placed at the distal point of stimulation of each nerve with cathode proximally. Maximum, minimum and mean F-wave latencies were then measured (Fig. 2).Fig. 1


Somatic neural alterations in non-diabetic obesity: a cross-sectional study
Representative trace of tibial distal and proximal compound muscle action potential
© Copyright Policy - OpenAccess
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC5120424&req=5

Fig1: Representative trace of tibial distal and proximal compound muscle action potential
Mentions: Once a recording was made, the trace was stored for later analysis and the stimulating electrode was moved proximally to the second site. The distance between stimulating electrodes at proximal and distal sites was measured with a measuring tape and was fed into the machine for nerve conduction velocity calculation. For each stimulation site, onset latency was measured in milliseconds from the stimulus artefact to the first deflection of CMAP whereas peak latency was measured at the midpoint of the first negative peak. CMAP amplitude was measured from baseline to the negative peak (base to peak) and duration of CMAP was measured from the onset to the final return of waveform to the baseline (Fig. 1). For recording F-response or the late response, the stimulator was placed at the distal point of stimulation of each nerve with cathode proximally. Maximum, minimum and mean F-wave latencies were then measured (Fig. 2).Fig. 1

View Article: PubMed Central - PubMed

ABSTRACT

Background: Reports 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.

Methods: The study was conducted on 30 adult non-diabetic obese persons (mean age 32.07 ± 7.25 years) with BMI > 30 Kg/m2 (mean BMI 30.02 ± 2.89 Kg/m2) and 29 age- and sex-matched normal weight controls (mean age 30.48 ± 8.01 years) with BMI: 18–24Kg/m2 (mean BMI 21.87 ± 2.40 Kg/m2). Nerve conduction study (NCS) variables of median, tibial and sural nerves were assessed in each subject using standard protocol. The data were compared by Mann Whitney ‘U’ test.

Results: In 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, p = 0.025] and bilateral tibial nerves [Right: 8.5(7.04–11.18) Vs 12.1(10.55–15) mV, p < 0.001 and left 9.08(6.58–11.65) Vs 13.05(10.2–15.6) mV, p = 0.002]. Furthermore, obese persons had prolonged CMAP durations of right and left median [10.5(9.62–12) Vs 10(8.4–10.3) ms, p = 0.02 and 10.85(10–11.88) Vs 10(9–10.57) ms, p = 0.019] and right tibial [10(9–11) 8.5(7.92–10) ms, p = 0.032] nerves. Sensory NCS (sural nerve) also showed diminished sensory nerve action potential (SNAP) amplitude [16(12.08–18.21) vs 22.8(18.3–31.08) μV, p < 0.001] and prolonged duration. However, onset latencies and conduction velocities for all nerves were comparable between the groups.

Conclusion: This 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.

No MeSH data available.