Oral diabetes-specific nutritional supplements (ONS-D) induce favourable postprandial responses in subjects with type 2 diabetes (DM2), but they have not been correlated yet with incretin release and subjective appetite (SA). This randomised, double-blind, cross-over study compared postprandial effects of ONS-D with isomaltulose and sucromalt versus standard formula (ET) on glycaemic index (GI), insulin, glucose-dependent insulinotropic polypeptide (GIP), glucagon-like peptide 1 (GLP-1) and SA in 16 individuals with DM2. After overnight fasting, subjects consumed a portion of supplements containing 25 g of carbohydrates or reference food. Blood samples were collected at baseline and at 30, 60, 90, 120, 150 and 180 min; and SA sensations were assessed by a visual analogue scale on separate days. Glycaemic index values were low for ONS-D and intermediate for ET (p < 0.001). The insulin area under the curve (AUC0–180 min) (p < 0.02) and GIP AUC (p < 0.02) were lower after ONS-D and higher GLP-1 AUC when compared with ET (p < 0.05). Subjective appetite AUC was greater after ET than ONS-D (p < 0.05). Interactions between hormones, hunger, fullness and GI were found, but not within the ratings of SA; isomaltulose and sucromalt may have influenced these factors.

Type 2 diabetes mellitus is a metabolic disorder that results from defects in both insulin secretion and insulin action. Questions remain about when insulin therapy is indicated; thus, the aim of this study was to evaluate homeostasis model assessment beta-cell (HOMAbetacell) values as surrogate criteria for insulin therapy indication in patients with type 2 diabetes. A prospective study was performed involving 189 type 2 diabetic patients with deficient metabolic control assessed by clinical and laboratory parameters. All patients received nutritional intervention and combination therapy with metformin and glimepiride. Patients who did not respond were admitted to the next phase, which consisted of glimepiride + metformin + rosiglitazone oral therapy and revaluation after 3 months. Comparisons between responders and nonresponders in this phase were made in order to achieve differences in metabolic parameters and beta cell function. Of 189 patients studied, 150 (79.36%) were considered full responders in the first phase of this study. The remaining 39 patients were admitted in the second trial phase, in which 20 patients (51.28%) responded to triple oral therapy, while the other 19 (49.72%) required insulin therapy. Significant differences were found in fasting and postprandial glycemia (P < 0.001; P < 0.004) between the non-insulin-requiring group (200 +/- 12.0 mg/dL; 266.05 +/- 17,67 mg/dL) and the insulin-requiring group (291.5 +/- 17.6 mg/dL; 361.6 +/- 26.1 mg/dL). Likewise, significant differences were observed in homeostasis model assessment insulin resistance (HOMAIR) and HOMAbetacell values (P < 0.002; P < 0.04) between non-insulin-requiring patients (7.7 +/- 0.8; 24.5 +/- 1.3%) and insulin-requiring patients (12.6 +/- 1.2; 19.4 +/- 2.4%). Finally, significant differences were observed when comparing body mass index (non-insulin-requiring group, 29.2 +/- 0.4 kg/m, versus insulin-requiring group, 27.1 +/- 0.9 kg/m; P < 0.05). HOMAbetacell determination in clinical practice is a useful tool to determine when insulin therapy should be started for type 2 diabetic patients.

Lipoprotein (a) [Lp(a)] was discovered by Kare Berg in 1963 from the study of low-density lipoprotein genetic variants. Lp(a) contains a unique protein, apolipoprotein(a), which is linked to the Apo B-100 through a disulfide bond that gives it a great structural homology with plasminogen, and confers it atherogenic and atherothrombotic properties. Interest in Lp(a) has increased because an important association between high plasma levels of Lp(a) and coronary artery disease and cerebral vascular disorders has been demonstrated. Numerous case control studies have confirmed that hyper-Lp(a) is a risk factor for premature cardiovascular disease. Lp(a) is identified as a genetic trait with autosomal transmission, codified by one of the most studied polymorphic genes in humans. It has been demonstrated that variations in this gene are a major factor in the serum levels of Lp(a). Variations differ considerably between individuals and sex across populations. Various approaches to drug treatment using fibric acid derivatives, growth hormone, insulin-like growth factor-1, alcohol extracted soy protein, niacin, and exercise have been proven to decrease Lp(a) in high risk patients, but none has really been an effective therapeutic option for successfully reducing Lp(a) plasma levels.

Coronary artery disease is the main cause of death worldwide. Lipoprotein(a) [Lp(a)], is an independent risk factor for coronary artery disease in which concentrations are genetically regulated. Contradictory results have been published about physical activity influence on Lp(a) concentration. This research aimed to determine associations between different physical activity levels and Lp(a) concentration. A descriptive and cross-sectional study was made in 1340 randomly selected subjects (males = 598; females = 712) to whom a complete clinical history, the International Physical Activity Questionnaire, and Lp(a) level determination were made. Statistical analysis was carried out to assess qualitative variables relationship by chi2 and differences between means by one-way analysis of variance considering a P value <0.05 as statistically significant. Results are shown as absolute frequencies, percentages, and mean +/- standard deviation according to case. Physical activity levels were ordinal classified as follows: low activity with 24.3% (n = 318), moderate activity with 35.0% (n = 458), and high physical activity with 40.8% (n = 534). Lp(a) concentration in the studied sample was 26.28 +/- 12.64 (IC: 25.59-26.96) mg/dL. Lp(a) concentration according to low, moderate, and high physical activity levels were 29.22 +/- 13.74, 26.27 +/- 12.91, and 24.53 +/- 11.35 mg/dL, respectively, observing statistically significant differences between low and moderate level (P = 0.004) and low and high level (P < 0.001). A strong association (chi2 = 9.771; P = 0.002) was observed among a high physical activity level and a normal concentration of Lp(a) (less than 30 mg/dL). A lifestyle characterized by high physical activity is associated with normal Lp(a) levels.

Latent Autoimmune Diabetes in Adults (LADA) is an autoimmune endocrine disorder in which despite the presence of antipancreatic islets antibodies in the moment of diagnostics, the progression to beta-cell secretory insufficiency is slow. It is often confused with others types of diabetes and therefore the management is frequently inadequate. We report a clinical case of a 23-year-old man with diagnosis of type 2 diabetes since 6 months ago, poorly controlled with a sulfonylurea, who initially presented 2 months ago from polyuria, polydipsia, and asthenia and 6 kg weight loss. History of past illness was negative, however, his mother relates exclusive breastfeeding during the first 15 days of life and later (until the 6 months) he was fed with infant formula (S-26). Family history revealed a first-degree relative (father) with diabetes mellitus secondary to steroid administration due to diagnosis of bone marrow hypoplasia. Also presents second-degree family history (uncle and grandfather) of type 2 diabetes mellitus. There were no pathologic findings at the physical examination. Anthropometry and laboratory tests were as follows: body mass index (BMI) = 19.66 kg/m, basal and postprandial glycemia = 108, and 276 mg/dL respectively, glycated haemoglobin = 8.9%, basal and postprandial C-peptide (2 hours) = 1.9, and 3.2 ng/mL, homeostasis model assessment of beta cell function: 87.5%, homeostasis model assessment of insulin resistance: 1.6. LADA presumptive diagnosis was confirmed with presence of autoantibodies anti-tyrosin-phosphatase and GAD65. At the time of diagnosis, individuals with LADA present an onset age <50, BMI <25 kg/m2, low magnitude postprandial and basal hyperglycemia, normal or close to normal C-peptide values, and thus not occur with acute hyperglycemic crises. Insulin therapy preserves pancreatic b-cell function, at the point that eventually prescribed insulin doses need to be reduced.