Weight loss in patients with types 1 and 2 diabetes is linked with an improvement in diabetic neuropathy, independent of blood glucose levels, according to results of a parallel-group study reported at the 75th Scientific Sessions of the American Diabetes Association meeting.
“To our knowledge, weight loss has not been shown previously to improve diabetic neuropathy,” stated lead author Adham Abdel Mottalib, MD, Joslin Diabetes Center, Boston, Massachusetts, speaking here on June 7. “It was previously shown that tight glycaemic control helps delay its onset,” he noted.
Dr. Mottalib and colleagues randomised 50 patients with diabetic neuropathy in a 1:1 fashion to either a 12-week multidisciplinary, intensive, lifestyle-intervention programme designed for clinical practice and focused on weight loss (mean haemoglobin A1C [HbA1C] 7.4 ± 1.2%, weight 240.7 ± 49.2 lbs, body mass index (BMI) 36.4 ± 5.6 kg/m2), or a control group that had no weight-loss intervention (mean HbA1C 7.6 ± 1.6%, weight 221.9 ± 38.9 lbs, BMI 35.8±5.3 kg/m2).
There were no differences between the 2 groups at baseline in terms of diabetic-neuropathy measures of sural nerve amplitude potential (SNAP) and conduction velocity (CV), assessed with a point-of-care nerve-conduction device.
At 6 months, the researchers observed that patients in the lifestyle-intervention group had a mean reduction in weight of 10.3±12.1 pounds and a reduction in HbA1C (-0.5 ± 0.6%); they observed no significant reduction in either measure in the patients in the control group.
While there were no significant differences between the groups in change in SNAP, CV was significantly increased only in the intervention group (+2.6 ± 4.9 m/s, P = 0.02).
At 12 months, while weight loss remained higher in the intervention group (-9.3 ±12.5 lbs) compared with the control group (-1.1 ± 9.2 lbs), HbA1C levels had returned to baseline in both groups.
Despite the reverting of HbA1C levels, the investigators observed SNAP reductions in both groups (-2.3 ± 5.1 μV, -1.3 ± 3 μV respectively, P < .05); however, CV continued to increase in the weight-loss intervention group (+4.4 ± 5.9 m/s, P = .001) while showing no change in the control group.
“We conclude that weight reduction is associated with improvement in peripheral-nerve conduction velocity,” Dr. Mottalib said. “This improvement is maintained despite [the] HbA1C return to baseline, indicating that this improvement is solely related to weight loss.”
Dr. Mottalib speculated that inflammation may play a role in the mechanism linking weight with neuropathic improvement. “It is known that weight loss is associated with the reduction of inflammatory markers. We think that this reduction gives peripheral nerves a chance to recover,” he remarked.