the growth of knowledge regarding the etiology and pathogenesis of diabetes has led many individuals and groups in the diabetes community to express the need for a revision of the nomenclature, diagnostic criteria, and classification of diabetes. As a consequence, it was deemed essential to develop an appropriate, uniform terminology and a functional, working classification of diabetes that reflects the current knowledge about the disease. (1)

Report of the expert committee on the diagnosis and classification of diabetes mellitus

Mounting evidence indicates that microglial activation contributes to neuronal damage in neurodegenerative diseases. Recent studies show that in response to certain environmental toxins and endogenous proteins, microglia can enter an overactivated state and release reactive oxygen species (ROS) that cause neurotoxicity. Pattern recognition receptors expressed on the microglial surface seem to be one of the primary, common pathways by which diverse toxin signals are transduced into ROS production. Overactivated microglia can be detected using imaging techniques and therefore this knowledge offers an opportunity not only for early diagnosis but, importantly, for the development of targeted anti-inflammatory therapies that might slow or halt the progression of neurodegenerative disease.

Microglia-mediated neurotoxicity: uncovering the molecular mechanisms

http://www.enfermeraspabellonyesterilizacion.cl/eventos/glycemic-index.pdf

International table of glycemic index and glycemic load values: 2002

This document represents the first collaboration between 2 organizations-the American Society for Parenteral and Enteral Nutrition and the Society of Critical Care Medicine-to describe best practices in nutrition therapy in critically ill children. The target of these guidelines is intended to be the pediatric critically ill patient (>1 month and 2-3 days in a PICU admitting medical, surgical, and cardiac patients. In total, 2032 citations were scanned for relevance. The PubMed/MEDLINE search resulted in 960 citations for clinical trials and 925 citations for cohort studies. The EMBASE search for clinical trials culled 1661 citations. In total, the search for clinical trials yielded 1107 citations, whereas the cohort search yielded 925. After careful review, 16 randomized controlled trials and 37 cohort studies appeared to answer 1 of the 8 preidentified question groups for this guideline. We used the GRADE criteria (Grading of Recommendations, Assessment, Development, and Evaluation) to adjust the evidence grade based on assessment of the quality of study design and execution. These guidelines are not intended for neonates or adult patients. The guidelines reiterate the importance of nutrition assessment-particularly, the detection of malnourished patients who are most vulnerable and therefore may benefit from timely intervention. There is a need for renewed focus on accurate estimation of energy needs and attention to optimizing protein intake. Indirect calorimetry, where feasible, and cautious use of estimating equations and increased surveillance for unintended caloric underfeeding and overfeeding are recommended. Optimal protein intake and its correlation with clinical outcomes are areas of great interest. The optimal route and timing of nutrient delivery are areas of intense debate and investigations. Enteral nutrition remains the preferred route for nutrient delivery. Several strategies to optimize enteral nutrition during critical illness have emerged. The role of supplemental parenteral nutrition has been highlighted, and a delayed approach appears to be beneficial. Immunonutrition cannot be currently recommended. Overall, the pediatric critical care population is heterogeneous, and a nuanced approach to individualizing nutrition support with the aim of improving clinical outcomes is necessary.

Guidelines for the Provision and Assessment of Nutrition Support Therapy in the Adult Critically Ill Patient Society of Critical Care Medicine (SCCM) and American Society for Parenteral and Enteral Nutrition (A.S.P.E.N.)

Increasing evidence in both experimental and clinical studies suggests that oxidative stress plays a major role in the pathogenesis of both types of diabetes mellitus. Free radicals are formed disproportionately in diabetes by glucose oxidation, nonenzymatic glycation of proteins, and the subsequent oxidative degradation of glycated proteins. Abnormally high levels of free radicals and the simultaneous decline of antioxidant defense mechanisms can lead to damage of cellular organelles and enzymes, increased lipid peroxidation, and development of insulin resistance. These consequences of oxidative stress can promote the development of complications of diabetes mellitus. Changes in oxidative stress biomarkers, including superoxide dismutase, catalase, glutathione reductase, glutathione peroxidase, glutathione levels, vitamins, lipid peroxidation, nitrite concentration, nonenzymatic glycosylated proteins, and hyperglycemia in diabetes, and their consequences, are discussed in this review. In vivo studies of the effects of various conventional and alternative drugs on these biomarkers are surveyed. There is a need to continue to explore the relationship between free radicals, diabetes, and its complications, and to elucidate the mechanisms by which increased oxidative stress accelerates the development of diabetic complications, in an effort to expand treatment options.

Diabetes, oxidative stress, and antioxidants: a review

To determine whether nutritional support guided by repeated measurements of resting energy requirements improves the outcome of critically ill patients. This was a prospective, randomized, single-center, pilot clinical trial conducted in an adult general intensive care (ICU) unit. The study population comprised mechanically ventilated patients (n = 130) expected to stay in ICU more than 3 days. Patients were randomized to receive enteral nutrition (EN) with an energy target determined either (1) by repeated indirect calorimetry measurements (study group, n = 56), or (2) according to 25 kcal/kg/day (control group, n = 56). EN was supplemented with parenteral nutrition when required. The primary outcome was hospital mortality. Measured pre-study resting energy expenditure (REE) was similar in both groups (1,976 ± 468 vs. 1,838 ± 468 kcal, p = 0.6). Patients in the study group had a higher mean energy (2,086 ± 460 vs. 1,480 ± 356 kcal/day, p = 0.01) and protein intake (76 ± 16 vs. 53 ± 16 g/day, p = 0.01). There was a trend towards an improved hospital mortality in the intention to treat group (21/65 patients, 32.3% vs. 31/65 patients, 47.7%, p = 0.058) whereas length of ventilation (16.1 ± 14.7 vs. 10.5 ± 8.3 days, p = 0.03) and ICU stay (17.2 ± 14.6 vs. 11.7 ± 8.4, p = 0.04) were increased. In this single-center pilot study a bundle comprising actively supervised nutritional intervention and providing near target energy requirements based on repeated energy measurements was achievable in a general ICU and may be associated with lower hospital mortality.

/pdf/the-tight-calorie-control-study-ticacos-a-prospective-512nhy40uu.pdf

The tight calorie control study (TICACOS): a prospective, randomized, controlled pilot study of nutritional support in critically ill patients

Insulin resistance is a predominant feature in women with polycystic ovarian syndrome (PCO). The cellular mechanisms for this insulin resistance have not been defined. In this study, major steps in the insulin action cascade, receptor binding, kinase activity, and glucose transport activity were evaluated in isolated adipocytes prepared from PCO subjects (n = 8) without acanthosis nigricans and in a group of age and weight-matched controls [normal cycling (NC) n = 8]. The PCO group was hyperinsulinemic and displayed elevated insulin responses to an iv glucose load. The binding of 125I-insulin to adipocytes was similar in cells from PCO and NC subjects. In PCO, autophosphorylation of the insulin receptor-subunit in the absence of insulin was normal but a significant decrease (30% below control) in maximal insulin stimulated autophosphorylation was observed. However, receptor kinase activity measured against the exogenous substrate poly glu:tyr (4:1) was normal. Cells from PCO subjects transported glucose a...

Cellular mechanisms of insulin resistance in polycystic ovarian syndrome.

Disruption of circadian rhythms leads to obesity and metabolic disorders. Timed restricted feeding (RF) provides a time cue and resets the circadian clock, leading to better health. In contrast, a high-fat (HF) diet leads to disrupted circadian expression of metabolic factors and obesity. We tested whether long-term (18 wk) clock resetting by RF can attenuate the disruptive effects of diet-induced obesity. Analyses included liver clock gene expression, locomotor activity, blood glucose, metabolic markers, lipids, and hormones around the circadian cycle for a more accurate assessment. Compared with mice fed the HF diet ad libitum, the timed HF diet restored the expression phase of the clock genes Clock and Cry1 and phase-advanced Per1, Per2, Cry2, Bmal1, Rorα, and Rev-erbα. Although timed HF-diet-fed mice consumed the same amount of calories as ad libitum low-fat diet-fed mice, they showed 12% reduced body weight, 21% reduced cholesterol levels, and 1.4-fold increased insulin sensitivity. Compared with the HF diet ad libitum, the timed HF diet led to 18% lower body weight, 30% decreased cholesterol levels, 10% reduced TNF-α levels, and 3.7-fold improved insulin sensitivity. Timed HF-diet-fed mice exhibited a better satiated and less stressed phenotype of 25% lower ghrelin and 53% lower corticosterone levels compared with mice fed the timed low-fat diet. Taken together, our findings suggest that timing can prevent obesity and rectify the harmful effects of a HF diet.

Timed high-fat diet resets circadian metabolism and prevents obesity

Olive oil is an integral ingredient of the Mediterranean diet and accumulating evidence suggests that it may have health benefits that include reduction of risk factors of coronary heart disease, prevention of several varieties of cancers, and modification of immune and inflammatory responses. Olive oil appears to be an example of a functional food, with varied components that may contribute to its overall therapeutic characteristics. Olive oil is known for its high levels of monounsaturated fatty acids and is also a good source of phytochemicals including polyphenolic compounds, squalene, and α-tocopherol.

Olive Oil as a Functional Food: Epidemiology and Nutritional Approaches

The effect of fenugreek on postprandial glucose and insulin levels following the meal tolerance test (MTT) was studied in non-insulin dependent diabetics (NIDDM). The addition of powdered fenugreek seed (15 g) soaked in water significantly reduced the subsequent postprandial glucose levels. The plasma insulin also tended to be lower in NIDDM given fenugreek but without a statistical difference. Fenugreek had no effect on lipid levels 3 h following the MTT. Fenugreek may have a potential benefit in the treatment of NIDDM.

Zecharia Madar

Papers

The tight calorie control study (TICACOS): a prospective, randomized, controlled pilot study of nutritional support in critically ill patients

Cellular mechanisms of insulin resistance in polycystic ovarian syndrome.

Timed high-fat diet resets circadian metabolism and prevents obesity

Olive Oil as a Functional Food: Epidemiology and Nutritional Approaches

Glucose-lowering effect of fenugreek in non-insulin dependent diabetics.