[Alimentary and lifestyle changes as a strategy in the prevention of metabolic syndrome and diabetes mellitus type 2: milestones and perspectives]. / Cambios alimentarios y de estilo de vida como estrategia en la prevención del síndrome metabólico y la diabetes mellitus tipo 2: hitos y perspectivas.

A high caloric intake in today's nutrition and a sedentary lifestyle are the main causes of the notable increase in obesity in our society. In turn, this results in an increase in associated pathologies, such as metabolic syndrome and diabetes type 2. In the present work we review most recent studies and programs, which are significant due to their sample size and geographical diversity. It clearly shows that changes in alimentation and lifestyles are an effective instrument for combatting or delaying the onset of these diseases. In this sense, prevention is also key to avoiding serious consequences related to diabetes and metabolic syndrome, which can affect the life of the population.

Postprandial insulin response and mitochondrial oxidation in obese men nutritionally treated to lose weight.

Obesity, hyperglycemia, and insulin resistance have been associated to an oxidative mitochondrial dysfunction. The aim of this research was to evaluate the relation between carbohydrate metabolism and mitochondrial oxidation, as affected by the weight status and the weight loss induced by a calorie-restricted diet. Lean control men (BMI<25 kg/m2, n = 6) and obese men (BMI>30 kg/m2, n = 14), who were characterized as insulin resistant (n = 6) or insulin sensitive (n = 8) based on HOMA index values, participated in the trial. Plasma insulin levels and mitochondrial oxidation estimated by the 2-keto(1-13C)isocaproate breath test, were measured after ingestion of a test meal during 3 h. Obese subjects repeated the breath test protocol after a 10-week caloric restriction diet to lose weight. Postprandial insulin secretion tended to be marginally higher (P = 0.059) in both obese groups than in controls, while the rate of postprandial mitochondrial oxidation was markedly decreased (P = 0.019) in the obese subjects as compared with lean individuals. The nutritionally induced weight loss produced a rise in the postprandial oxidative process in volunteers initially considered as insulin resistant (P = 0.036), while no statistical differences in the insulin-sensitive obese (P = 0.241) were found. Interestingly, the percentage of oxidized tracer was inversely related to postprandial insulin secretion (r = -0.56; P = 0.001). In conclusion, these results support the hypothetized relation between carbohydrate metabolism and mitochondrial oxidation at a postprandial state in obese subjects, raising interest about mitochondria stimulation as a target in the therapy of obesity.

[In vivo study of mitochondrial oxidation in obese patients treated by means of calorie restriction]. / Estudio in vivo de la oxidación mitocondrial en pacientes obesos tratados mediante restricción calórica.

The energy restriction is the most common nutritional approach to treat obesity, whose efficiency depends on oxidative response against changes in body weight. In that context, the aim of the present work was to in vivo examine the mitochondrial oxidation of obese volunteers by the 2-keto[1-(13)C]isocaproate breath test, before and after weight loss. Thirty-two volunteers (men and women) participated: 16 controls (body mass index: 19.0-27.0 kg/m2), and 16 obese (body mass index: 30.0-41.6 kg/m2) who followed a caloric restriction program for 10 weeks (-500 kcal). Before and after dieting, the 2-keto[1-(13)C]isocaproate breath test was performed by ingestion of 1 mg/kg tracer and 20 mg/kg L-leucine, dissolved in 200 ml orange juice. Breath samples were recovered at baseline and at 10 min intervals for 2 h after ingestion. The 13C-enrichment in breath was measured by isotope ratio mass spectrometry and the percentage of mitochondrial oxidation of tracer (%13C) was calculated. The percentage of oxidized tracer marginally tended to be lower in obese than in controls (25.1 +/- 5.5%, vs 27.5 +/- 4.0%, p = 0.175). After the intervention, the mean of weight loss was -7.8% +/- 3% p < 0.001), and the mitocondrial oxidation of the tracer statistically increased (25.1 +/- 5.5% vs 34.3 +/- 5.2%, p < 0.001). In fact, the body weight and the percentage of oxidized 2-keto[1-(13)C]isocaproate were inversely related (r = -0.34, p = 0.018). Thus, the 2-keto[1-(13)C]isocaproate in vivo showed the mitochondrial adaptation of obese volunteers treated by caloric-restriction intake and provided new information about the weight loss process induced by an hypocaloric diet.

Daily ingestion of fermented milk containing Lactobacillus casei DN114001 improves innate-defense capacity in healthy middle-aged people.

Different lactic acid bacteria have often been administered as a dietary means to enhance immune system activity. Based on this statement, the aim of the current work was to test the effects of a Lactobacillus casei DN114001 fermented milk consumption on the immune response capacity in middle-age volunteers. Forty-five healthy volunteers, 24 women and 21 men (aged: 51-58 years), were randomized into two groups to receive three cups per day of a L. casei DN114001 (10(8)-10(10) ufc/g) fermented milk (n = 23), or placebo (n = 22), during an 8-week period. Measurements were performed before (day 0), and after the nutritional intervention (day 56). After the trial, no changes in immune cell proportions were detected, but the probiotic-treated group increased oxidative burst capacity of monocytes (probiotic group: p = 0.029; placebo group: p = 0.625), as well as NK cells tumoricidal activity (probiotic group: p = 0.023; placebo group: p = 0.125). Results showed that daily intake of fermented milk containing Lactobacillus casei DN114001 could have a positive effect in modulating the innate immune defense in healthy-middle-age people.