Almurdhi Monirah M, Reeves Neil D, Bowling Frank L, Boulton Andrew J M, Jeziorska Maria, Malik Rayaz A
Centre for Endocrinology and Diabetes, Institute of Human Development, Central Manchester University Hospitals NHS Foundation Trust, Manchester Academic Health Science Centre, Manchester, U.K.
School of Healthcare Science, Faculty of Science and Engineering, Manchester Metropolitan University, Manchester, U.K.
Diabetes Care. 2016 Mar;39(3):441-7. doi: 10.2337/dc15-0995. Epub 2016 Jan 6.
Muscle weakness and atrophy of the lower limbs may develop in patients with diabetes, increasing their risk of falls. The underlying basis of these abnormalities has not been fully explained. The aim of this study was to objectively quantify muscle strength and size in patients with type 2 diabetes mellitus (T2DM) in relation to the severity of neuropathy, intramuscular noncontractile tissue (IMNCT), and vitamin D deficiency.
Twenty patients with T2DM and 20 healthy control subjects were matched by age, sex, and BMI. Strength and size of knee extensor, flexor, and ankle plantar and dorsiflexor muscles were assessed in relation to the severity of diabetic sensorimotor polyneuropathy (DSPN), amount of IMNCT, and serum 25-hydroxyvitamin D (25OHD) levels.
Compared with control subjects, patients with T2DM had significantly reduced knee extensor strength (P = 0.003) and reduced muscle volume of both knee extensors (P = 0.045) and flexors (P = 0.019). Ankle plantar flexor strength was also significantly reduced (P = 0.001) but without a reduction in ankle plantar flexor (P = 0.23) and dorsiflexor (P = 0.45) muscle volumes. IMNCT was significantly increased in the ankle plantar (P = 0.006) and dorsiflexors (P = 0.005). Patients with DSPN had significantly less knee extensor strength than those without (P = 0.02) but showed no difference in knee extensor volume (P = 0.38) and ankle plantar flexor strength (P = 0.21) or volume (P = 0.96). In patients with <25 nmol/L versus >25 nmol/L 25OHD, no significant differences were found for knee extensor strength and volume (P = 0.32 vs. 0.18) and ankle plantar flexors (P = 0.58 vs. 0.12).
Patients with T2DM have a significant reduction in proximal and distal leg muscle strength and a proximal but not distal reduction in muscle volume possibly due to greater intramuscular fat accumulation in distal muscles. Proximal but not distal muscle strength is related to the severity of peripheral neuropathy but not IMNCT or 25OHD level.
糖尿病患者可能会出现下肢肌肉无力和萎缩，从而增加其跌倒风险。这些异常情况的潜在原因尚未完全阐明。本研究的目的是客观量化2型糖尿病（T2DM）患者的肌肉力量和大小，并分析其与神经病变严重程度、肌内非收缩性组织（IMNCT）以及维生素D缺乏之间的关系。
选取20例T2DM患者和20名健康对照者，按照年龄、性别和体重指数进行匹配。评估膝伸肌、屈肌以及踝跖屈肌和背屈肌的力量和大小，并分析其与糖尿病感觉运动性多发性神经病变（DSPN）的严重程度、IMNCT量以及血清25-羟基维生素D（25OHD）水平之间的关系。
与对照者相比，T2DM患者的膝伸肌力量显著降低（P = 0.003），膝伸肌（P = 0.045）和屈肌（P = 0.019）的肌肉体积均减小。踝跖屈肌力量也显著降低（P = 0.001），但踝跖屈肌（P = 0.23）和背屈肌（P = 0.45）的肌肉体积未减小。踝跖屈肌（P = 0.006）和背屈肌（P = 0.005）的IMNCT显著增加。患有DSPN的患者膝伸肌力量明显低于未患DSPN的患者（P = 0.02），但膝伸肌体积（P = 0.38）、踝跖屈肌力量（P = 0.21）或体积（P = 0.96）无差异。25OHD水平<25 nmol/L与>25 nmol/L的患者相比，膝伸肌力量和体积（P = 0.32对0.18）以及踝跖屈肌（P = 0.58对0.12）均无显著差异。
T2DM患者的近端和远端腿部肌肉力量显著降低，肌肉体积近端减小但远端未减小，这可能是由于远端肌肉中肌内脂肪堆积更多。近端而非远端肌肉力量与周围神经病变的严重程度有关，与IMNCT或25OHD水平无关。
