OBJECTIVE: This cross-sectional study was aimed to investigate the isolated influence of obesity on peripheral sensorimotor and autonomic neuropathy in patients with long-term non-insulin-dependent diabetes mellitus (NIDDM). RESEARCH DESIGN AND METHODS: Ninety-one long-term NIDDM patients with a mean duration of 13.6 +/- 1.0 years and a mean age of 60.4 +/- 1.0 years were divided into two groups according to their body mass index (BMI) (lean with a BMI < 26.5: n = 41, age = 58.6 +/- 1.7 years, BMI = 23.7 +/- 0.3 kg/m2; and obese with a BMI > or = 26.5: n = 50, age = 61.9 +/- 1.2 years, BMI = 30.5 +/- 0.5 kg/m2). The two groups were not different in age, duration, gender, current parameters of glycemic control, number of smokers, cholesterol, triglycerides, and systolic and diastolic blood pressure. Neuropathic late complications were scrutinized by a standardized clinical examination that delivers a neuropathy score, pupillary autonomic neuropathy assessed by pupillometry, and cardiovascular autonomic neuropathy using a standardized test battery. RESULTS: One-way analysis of variance revealed that obese patients had poor results in the clinical neuropathy test (overall score in obese vs. lean: 71.1 +/- 2.9 vs. 80.6 +/- 3.0 points, 2P = 0.0266; 100 points were absolutely normal). This was particularly true for the discrimination perception (obese vs. lean: 67.0 +/- 4.0 vs. 81.7 +/- 3.3 points, 2P = 0.0073) and the reflex status (obese vs. lean: 57.4 +/- 4.0 vs. 71.8 +/- 4.3 points, 2P = 0.0164). Furthermore, obese patients had a poor result in the respiratory sinus arrhythmia (RSA) test, one of six autonomic function tests (RSA: obese vs. lean in average RSA percentile: 36.9 +/- 4.9 vs. 54.0 +/- 5.9%, 2P = 0.0264). CONCLUSIONS: Obesity influences sensorimotor and autonomic neuropathic late complications. The poor result in RSA in obesity may indicate an interrelation between pathogenesis of obesity and disorders of the respiratory and heart rhythm-generating control centers in the brain stem. Moreover, it could be due to intrathoracic fat deposits that alter lung mobility. Body mass control may be an important approach to reduce neuropathic complications. Beyond that, it seems necessary to control for body mass when comparing neuropathy in two groups of patients with NIDDM.
OBJECTIVE: This cross-sectional study was aimed to investigate the isolated influence of obesity on peripheral sensorimotor and autonomic neuropathy in patients with long-term non-insulin-dependent diabetes mellitus (NIDDM). RESEARCH DESIGN AND METHODS: Ninety-one long-term NIDDMpatients with a mean duration of 13.6 +/- 1.0 years and a mean age of 60.4 +/- 1.0 years were divided into two groups according to their body mass index (BMI) (lean with a BMI < 26.5: n = 41, age = 58.6 +/- 1.7 years, BMI = 23.7 +/- 0.3 kg/m2; and obese with a BMI > or = 26.5: n = 50, age = 61.9 +/- 1.2 years, BMI = 30.5 +/- 0.5 kg/m2). The two groups were not different in age, duration, gender, current parameters of glycemic control, number of smokers, cholesterol, triglycerides, and systolic and diastolic blood pressure. Neuropathic late complications were scrutinized by a standardized clinical examination that delivers a neuropathy score, pupillary autonomic neuropathy assessed by pupillometry, and cardiovascular autonomic neuropathy using a standardized test battery. RESULTS: One-way analysis of variance revealed that obesepatients had poor results in the clinical neuropathy test (overall score in obese vs. lean: 71.1 +/- 2.9 vs. 80.6 +/- 3.0 points, 2P = 0.0266; 100 points were absolutely normal). This was particularly true for the discrimination perception (obese vs. lean: 67.0 +/- 4.0 vs. 81.7 +/- 3.3 points, 2P = 0.0073) and the reflex status (obese vs. lean: 57.4 +/- 4.0 vs. 71.8 +/- 4.3 points, 2P = 0.0164). Furthermore, obesepatients had a poor result in the respiratory sinus arrhythmia (RSA) test, one of six autonomic function tests (RSA: obese vs. lean in average RSA percentile: 36.9 +/- 4.9 vs. 54.0 +/- 5.9%, 2P = 0.0264). CONCLUSIONS:Obesity influences sensorimotor and autonomic neuropathic late complications. The poor result in RSA in obesity may indicate an interrelation between pathogenesis of obesity and disorders of the respiratory and heart rhythm-generating control centers in the brain stem. Moreover, it could be due to intrathoracic fat deposits that alter lung mobility. Body mass control may be an important approach to reduce neuropathic complications. Beyond that, it seems necessary to control for body mass when comparing neuropathy in two groups of patients with NIDDM.
Authors: J Robinson Singleton; Robin L Marcus; Margaret K Lessard; Justin E Jackson; A Gordon Smith Journal: Ann Neurol Date: 2014-12-04 Impact factor: 10.422
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Authors: Brian C Callaghan; Rong Xia; Mousumi Banerjee; Nathalie de Rekeneire; Tamara B Harris; Anne B Newman; Suzanne Satterfield; Ann V Schwartz; Aaron I Vinik; Eva L Feldman; Elsa S Strotmeyer Journal: Diabetes Care Date: 2016-03-10 Impact factor: 19.112
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