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Summary This systematic review aimed at addressing the ursolic acid actions as an adjunctive treatment of the obesity-mediated metabolic abnormalities. To explore our aims, we used the literature search including clinical and animal studies using the Medline and Google Scholar (up to December 2015). Out of 63 screened studies, 17 presented eligibility criteria, such as the use of ursolic acid on adiposity, energy expenditure and skeletal muscle mass in mice and humans. In the literature, we found that several physiological and molecular mechanisms are implicated in the effects of ursolic acid on obesity, energy expenditure, hepatic steatosis, skeletal muscle mass loss and physical fitness, such as (1) increase of thermogenesis by modulation adipocyte transcription factors, activation of 5′ adenosine monophosphate-activated protein kinase and overexpression of the uncoupling protein 1 thermogenic marker; (2) enhancement of skeletal muscle mass by activation in bloodstream growth hormone and insulin-like growth factor-1 concentrations secretion, as well as in the activation of mammalian target of rapamycin and inhibition of ring-finger protein-1; and (3) improvement of physical fitness by skeletal muscle proliferator-activated receptor gamma co-activator alpha and sirtuin 1 expression. Therefore, supplementation with ursolic acid may be an adjunctive therapy for prevention and treatment of obesity-mediated and muscle mass-mediated metabolic consequences.

This review emphasizes the role of a timely supplemental parenteral nutrition (PN) for critically ill patients. It contradicts the recommendations of current guidelines to avoid the use of PN, as it is associated with risk. Critical illness results in severe metabolic stress. During the early phase, inflammatory cytokines and mediators induce catabolism to meet the increased body energy demands by endogenous sources. This response is not suppressed by exogenous energy administration, and the early use of PN to reach the energy target leads to overfeeding. On the other hand, early and progressive enteral nutrition (EN) is less likely to cause overfeeding because of variable gastrointestinal tolerance, a factor frequently associated with significant energy deficit. Recent studies demonstrate that adequate feeding is beneficial during and after the intensive care unit (ICU) stay. Supplemental PN allows for timely adequate feeding, if sufficient precautions are taken to avoid overfeeding. Indirect calorimetry can precisely define the adequate energy prescription. Our pragmatic approach is to start early EN to progressively test the gut tolerance and add supplemental PN on day 3 or 4 after ICU admission, only if EN does not meet the measured energy target. We believe that supplemental PN plays a pivotal role in the achievement of adequate feeding in critically ill patients with intolerance to EN and does not cause harm if overfeeding is avoided by careful prescription, ideally based on energy expenditure measured by indirect calorimetry.

Malnutrition is common at hospital admission and tends to worsen during hospitalization. This controlled population study aimed to determine if serum albumin or moderate and severe nutritional depletion by Nutritional Risk Index (NRI) at hospital admission are associated with increased length of hospital stay (LOS) (and increased hospital cost) in patients admitted to hospitals in 2 European countries.Serum albumin levels and recent weight loss were prospectively determined at hospital admission in Geneva (n = 652) and Berlin (n = 621). Patients were classified as no, mild, moderate or severe risk by NRI. Multiple logistic regressions were used to determine the association between albumin and nutritional risk category and LOS.Patients (24%) were at moderate or severe nutritional risk by NRI. Nutritional risk by NRI, adjusted for age, was associated with LOS of 11 days (moderate: odds ratio [OR] 1.9, 95% confidence interval [CI] 1.4 to 2.7, p.005; severe: OR 2.9, 95% CI 1.6 to 5.3, p.005). Serum albumin was also significantly associated with increased LOS (p.001).The prevalence of nutritional depletion assessed by NRI and albumin was increased with longer LOS. Albumin alone underestimated nutritional risk. Severe nutritional depletion by NRI was significantly associated with LOSor = 11 days in Geneva and Berlin patients. Nutrition screening should take place at hospital admission to determine nutritional risk and risk for longer LOS.

Cigarette smoke contains many xenobiotics, including oxidants and free radicals, which can increase lipid peroxidation. Recently, breath pentane output (BPO) has been recognized as a good indicator of lipid peroxidation. Vitamin E is known to be a potent free radical scavenger which can protect biological membranes against oxidative damage. We investigated the effect of vitamin E (dl-alpha-tocopherol) on lipid peroxidation in 13 healthy smokers. The results showed (1) smokers had increased BPO as compared with 19 healthy non-smokers (16.3 +/- 1.9 vs 5.8 +/- 0.5, pmol/kg body weight/min, p less than 0.001) although both groups had comparable plasma vitamin E and selenium concentrations, (2) supplementation with vitamin E (800 mg/day for 2 weeks) decreased BPO in smokers, and (3) the concentration of plasma selenium-dependent glutathione peroxidase was restored to normal in those smokers (five out of 13) in whom this was low initially. We conclude that a normal plasma concentration of vitamin E does not prevent this increase of lipid peroxidation in smokers but that substantial doses of vitamin E will significantly reduce this increased lipid peroxidation. If a major function of vitamin E is to protect lipids from peroxidation, then smokers have a conditioned insufficiency of vitamin E on a normal diet.