RESUMEN
BACKGROUND: Liraglutide has well-known effects on glucose patterns. However, its several other metabolic properties are still controversial. Given this background, the aims of the present study are to evaluate the effects of 24-week liraglutide treatment on body composition, appetite, and lipid profile in overweight and obese type 2 diabetes mellitus (T2DM) patients. METHODS: A cohort study was carried out on overweight and obese T2DM patients with glycosylated hemoglobin A1c equal to 6% (42 mmol/mol)-10% (86 mmol/mol), under a 3-month treatment (at least) with maximal dose of metformin as stable regime, by adding liraglutide at doses up to 3 mg/d. Body composition markers were measured by dual-energy X-ray densitometry at baseline and after 24 weeks of liraglutide treatment. Glucose control was monitored by glucose, glycosylated hemoglobin A1c, insulin, and homeostasis model assessment. Finally, the appetite sensation and plasma lipids were also evaluated. RESULTS: Twenty-eight subjects (male/female: 16/12, mean age: 58.75±9.33 years, body mass index: 34.13±5.46 kg/m(2)) were evaluated. Accounting for the adjustment for age, sex, and duration of diabetes, we noted significant decreases in body mass index (-0.86 kg/m(2), P=0.024), fat mass (-2.01 kg, P=0.015), fat mass index (-0.71 kg/m(2), P=0.014), android fat (-1.72%, P=0.022), trunk fat (-1.52%, P=0.016), and waist circumference (-6.86 cm, P<0.001) from the baseline values. Haber score was increased by 3.82 units (P=0.009), and the number of metabolic syndrome risk factors was decreased (-0.69 units, P=0.012). The glucose control variables and total cholesterol/high-density lipoprotein cholesterol ratio also showed significant decreases from baseline values. CONCLUSION: The 24-week liraglutide treatment leads to the reduction of fat mass, android fat, trunk fat, and appetite by improving the lipid profile, glucose control, and insulin sensitivity.
RESUMEN
Neuropathy and peripheral artery disease represent the main pathophysiological conditions underlying diabetic foot. Several studies showed that Lipoprotein(a)-Lp(a)-and homocysteine (Hcy) can be associated with diabetic complications, but their relationship with diabetic foot is unclear. Aim of this study was to investigate whether Lp(a) and Hcy were associated with diabetic foot ulcerations, classified according to the presence of peripheral artery disease (PAD) or neuropathy. From among consecutive type 2 diabetic attending at the Diabetic Foot Clinic 27 subjects with vascular diabetic foot (VDF), 43 with neuropathic diabetic foot (NDF) and 52 controls without foot ulceration, neuropathy, and PAD were enrolled. Both Lp(a) (26.1 ± 22.7 vs. 14.9 ± 19.5 mg/dl; P = 0.003) and Hcy levels (15.4 ± 5.7 vs. 12.2 ± 5.1 µmol/l; P = 0.022) were significantly greater in the VDF group than in controls. Lp(a) levels were significantly lower in the NDF group than in controls (6.9 ± 8.1 versus 14.9 ± 19.5 mg/dl; P = 0.009), while no difference in Hcy levels was found. Multiple logistic regression analysis showed that Hcy was associated with VDF (OR: 1.11; 95% CI: 1.07-14.1; P = 0.048). Lp(a) did not enter the model, but its P-value was very near to the significant level (OR: 1.09; 95% CI: 0.99-12.05; P = 0.059). Moreover, low Lp(a) levels were associated with NDF (OR: 0.84; 95% CI: 0.21-0.96; P = 0.039). Our study has shown for the first time that high Lp(a) and Hcy levels are associated with the development of VDF, while low Lp(a) levels appear to be associated with delayed wound healing in patients with neuropathic foot ulcerations.