Foot infections are frequent and potentially devastating complications of diabetes. Unchecked, infection can progress contiguously to involve the deeper soft tissues and ultimately the bone. Foot ulcers in people with diabetes are most often the consequence of one or more of the following: peripheral sensory neuropathy, motor neuropathy and gait disorders, peripheral arterial insufficiency or immunological impairments. Infection develops in over half of foot ulcers and is the factor that most often leads to lower extremity amputation. These amputations are associated with substantial morbidity, reduced quality of life and major financial costs. Most infections can be successfully treated with optimal wound care, antibiotic therapy and surgical procedures. Employing evidence-based guidelines, multidisciplinary teams and institution-specific clinical pathways provides the best approach to guide clinicians through this multifaceted problem. All clinicians regularly seeing people with diabetes should have an understanding of how to prevent, diagnose and treat foot infections, which requires familiarity with the pathophysiology of the problem and the literature supporting currently recommended care.

Increased EC plasma levels of AEA and 2-AG are associated with coronary circulatory dysfunction in obese individuals. This observation might suggest increases in EC plasma levels as a novel endogenous cardiovascular risk factor in obesity, but needing further investigations.

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Objective: To assess the relationships between BMI and walking speed, balance control, sit-to-stand performance (a measure of mass specific lower limb power), and endurance. Design and Methods: Thirty-six women with a BMI 30 kg/m 2 and 10 women with normal body weight (BMI between 18 kg/m 2 and 25 kg/m 2 ) were enrolled in this observational study. The obese group comprised 12 persons with a BMI 30 and <35 (obese), 14 subjects with a BMI 35 and <40 (severe obesity) and 10 people with a BMI 40 kg/m 2 (morbid obesity). All subjects underwent a clinical examination, a gait test, an endurance test (6 minutes walking test), a mass specific lower limb power test (five times sit-to-stand) and a balance test. Results: Obese women exhibited slower fast gait speeds (P < 0.05) with correspondingly shorter stride lengths, poorer sit-to-stand performance (P < 0.05), and endurance (P < 0.05). However, once the state of severe obesity was reached, additional weight gain (morbid obesity) does not seem to decrease these functional capacities any further.Conclusion: This study underlines the importance of assessing obese patients' related physical problems in an early stage of obesity in order to focus exercise regimens and promote appropriate health behaviors.

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Terminal augmented feedback training may positively affect motor learning in diabetic patients with peripheral neuropathy and could possibly lead to suitable foot offloading. Additional research is needed to confirm the maintenance of offloading in the long term.

Subsets of obese subjects without any cardiometabolic risk factors have been repeatedly described. This raises questions whether obesity 'per se' enhances the risk for cardiovascular or metabolic diseases and whether healthy obese subjects would benefit from a medical treatment. In order to answer these questions, as a first step, an expert consensus should be reached for the definition of metabolic normality. In fact, up to now, different parameters related to the metabolic syndrome and/or to insulin sensitivity have been utilized across studies. Once an agreement is reached, population-based studies should be undertaken to establish the incidence of metabolic normality among obese subjects. Furthermore, many other parameters such as age, sex, race, fat distribution and physical activity should be monitored to obtain results representative of a general population. Longitudinal studies aimed at investigating the evolution of the cardiometabolic profile of healthy obese subjects are also needed. In conclusion, data from the literature strongly suggest that a regular surveillance of the cardiometabolic parameters and a prevention of any further weight gain should be applied to healthy obese individuals, whereas possible benefits of a weight loss treatment are still a matter of debate.

Objective— The dyslipidemia of type 2 diabetes mellitus has multiple etiologies and impairs lipoprotein functionality, thereby increasing risk for cardiovascular disease. High-density lipoproteins (HDLs) have several beneficial effects, notably protecting the heart from myocardial ischemia. We hypothesized that glycation of HDL could compromise this cardioprotective effect. Approach and Results— We used in vitro (cardiomyocytes) and ex vivo (whole heart) models subjected to oxidative stress together with HDL isolated from diabetic patients and nondiabetic HDL glycated in vitro (methylglyoxal). Diabetic and in vitro glycated HDL were less effective ( P <0.05) than control HDL in protecting from oxidative stress. Protection was significantly, inversely correlated with the degree of in vitro glycation ( P <0.001) and the levels of hemoglobin A1c in diabetic patients ( P <0.007). The ability to activate protective, intracellular survival pathways involving Akt, Stat3, and Erk1/2 was significantly reduced ( P <0.05) using glycated HDL. Glycation reduced the sphingosine-1-phosphate (S1P) content of HDL, whereas the S1P concentrations of diabetic HDL were inversely correlated with hemoglobin A1c ( P <0.005). The S1P contents of in vitro glycated and diabetic HDL were significantly, positively correlated (both <0.01) with cardiomyocyte survival during oxidative stress. Adding S1P to diabetic HDL increased its S1P content and restored its cardioprotective function. Conclusions— Our data demonstrate that glycation can reduce the S1P content of HDL, leading to increased cardiomyocyte cell death because of less effective activation of intracellular survival pathways. It has important implications for the functionality of HDL in diabetes mellitus because HDL-S1P has several beneficial effects on the vasculature.