Malnutrition in type 2 diabetic patients does not affect healing of foot ulcers.

AIM: Protein-energy malnutrition is known to be involved in wound healing. While wound healing in patients with diabetic foot ulcers (DFU) is a complex and multifactorial process, the role of malnutrition in this case has rarely been explored. The objective of this study was to determine whether the nutritional status of diabetic patients influences the healing of DFU. METHODS: 48 patients were included in this prospective, single-center study. All patients with comorbidities or factors involving malnutrition or influencing biological measurements were excluded. Patients were followed up for 24 weeks. RESULTS: The malnutrition rate was 29.2% at baseline and 25.6% at the end of the study. The difference was not significant. Of the 35 patients with wound healing, 29% were undernourished at inclusion and 17% at the end of the study. Of the 12 patients without wound healing, 50% were undernourished at inclusion, and 42% at the end of the study. These differences were not significant. Rate and speed of wound healing were not associated with malnutrition at inclusion. 15% of patients without malnutrition at baseline had final malnutrition. CONCLUSION: We demonstrated that wound healing was not affected by the initial presence of malnutrition. In our study, there is no evidence to support nutritional intervention to improve wound healing in diabetic patients. Nevertheless, malnutrition is responsible for an increase in morbidity and mortality and it is essential to identify malnutrition systematically for all patients with DFU, initially and during follow-up to treat it quickly and efficiently.

Type A competitiveness traits correlate with downregulation of c-Fos expression in patients with type 1 diabetes.

AIM: Type A personality has been associated with increased survival in people with type 1 diabetes (T1D). Systemic low-grade inflammation may play a critical role, as suggested in recent reports, although the links between the inflammatory circulating transcriptome and Type A remain unknown. This prompted our exploration of the potential associations between Type A personality and c-Fos gene expression, a candidate gene closely linked to inflammatory processes, in T1D. METHODS: Type A personality was assessed by Bortner questionnaire in patients with T1D, and two subscales - 'speed' and 'competitiveness' - were used to measure these specific dimensions of Type A. Expression of the c-Fos gene was assessed by a quantitative real-time polymerase chain reaction technique. RESULTS: This pilot study included 20 men with T1D. Multivariable analyses showed an independent inverse association between Type A competitiveness score and c-Fos expression, while a regression model adjusted for age, body mass index and HbA1c levels revealed a significant inverse relationship between c-Fos transcripts and Type A competitiveness (P = 0.003). CONCLUSION: This strong association between Type A competitiveness and reduced c-Fos expression is in line with recent data suggesting a psychobiological influence of the Type A profile in T1D via inflammatory pathways.

Potential influence of Type A personality on plasma C-reactive protein levels in people with diabetes.

AIM: Type A personality, although classically known as a factor linked to increased vascular risk, has recently been associated with increased survival in patients with diabetes. As low-grade inflammation predicts a poor outcome, the present study explored the potential associations between Type A and plasma levels of C-reactive protein (CRP) in diabetes. METHODS: Type A personality was assessed by the Bortner questionnaire in people with diabetes. The association between Type A and plasma CRP levels was examined by multivariable linear regression, and structural equation modelling (SEM) was performed to determine the impact of the major clinical, biological and psychological confounders. RESULTS: The study included 626 participants with type 1 and type 2 diabetes from the Diabetes and Psychological Profile study. Multivariable analyses showed an independent inverse association between Type A score and CRP levels. The structural model adjusted for age, gender, diabetes type and duration, body mass index (BMI), smoking status, alcohol abuse, oral antidiabetic and statin treatments, HbA1c levels, lipids, perceived stress, anxiety and depression revealed significant associations between CRP and Type A (ß=-0.135, 95% CI: -0.242, -0.028; P=0.014), BMI (ß=0.194, 95% CI: 0.038, 0.350; P=0.015) and HDL cholesterol (ß=-0.132, 95% CI: -0.245, -0.020; P=0.014). CONCLUSION: Our present study data indicate that Type A personality is independently associated with lower CRP levels. This lower level of inflammation might explain the better clinical outcomes associated with Type A personality in patients with diabetes.

The cannabinoid agonist WIN55,212-2 suppresses opioid-induced emesis in ferrets.

BACKGROUND: Cannabinoid receptor agonists reverse nausea and vomiting produced by chemotherapy and radiation therapy in animals and humans but have not been tested against opioid-induced emesis. This study tests the hypothesis that cannabinoid receptor agonists will prevent opioid-induced vomiting. METHODS: Twelve male ferrets were used. They weighed 1.2-1.6 kg at the beginning and 1.8-2.3 kg at the end of the experiments. All drugs were injected subcutaneously. WIN55,212-2, a mixed CB1-CB2 cannabinoid receptor agonist, was administered 25 min before morphine. Retches and vomits were counted at 5-min intervals for 30 min after morphine injection. RESULTS: Retching and vomiting responses increased with increasing morphine doses up to 1.0 mg/kg, above which the responses decreased. Previous administration of naloxone prevented morphine-induced retching and vomiting. WIN55,212-2 dose-dependently reduced retching and vomiting. The ED50 was 0.05 mg/kg for retches and 0.03 mg/kg for vomits. At 0.13 mg/kg, retching decreased by 76% and vomiting by 92%. AM251, a CB1 receptor-selective antagonist, blocked the antiemetic actions of WIN55,212-2, but AM630, a CB2 receptor-selective antagonist, did not. CONCLUSIONS: These results demonstrate that WIN55,212-2 prevents opioid-induced vomiting and suggest that the antiemetic activity of WIN55,212-2 occurs at CB1 receptors. This is consistent with findings that CB1 receptors are the predominant cannabinoid receptors in the central nervous system and that antiemetic effects of cannabinoids appear to be centrally mediated.