APOA1 (-75 G>A and 83 C>T) and APOB (2488 C>T) polymorphisms and their association with myocardial infarction, lipids and apolipoproteins in patients with type 2 diabetes mellitus.

Introduction: The increased risk of myocardial infarction (MI) in type 2 diabetes mellitus (T2DM) is well documented. Polymorphisms in APOA1 and APOB genes allow us to identify new genetic markers in the Mexican population with T2DM and MI. Material and methods: We studied 135 patients with DMT2 and MI (DI); another 85 non-infarcted diabetic individuals with DMT2 but without previous ischemic events (NID) and 242 healthy subjects (HS). All three groups were selected with the aim to investigate the association between the polymorphisms and infarction when T2DM is present or absent. Results: -75 G>A polymorphism: Differences were found in genotype distribution between DI and NID individuals (OR = 2.01, 95% CI: 1.117-3.623, p = 0.019) with an increased risk for A in the dominant model (OR = 1.77, 95% CI: 1.020-3.084, p = 0.042); also concentrations of ApoA-I for A/A were lower in comparison with G/A (p = 0.038) and LDL-C and HDL-C levels were lower in G/A compared to G/G carriers. 83 C>T polymorphism of APOA1: For DI individuals, HDL-C was lower in T/T compared to C/C and triglyceride levels were lower in C/T compared to C/C carriers. Conclusions: The -75 G>A APOA1 polymorphism could be considered as a susceptibility factor for myocardial infarction in individuals with T2DM and 2488 C>T APOB polymorphism is associated with changes in HDL-C and LDL-C and triglycerides in the same group.

Appetite-regulating hormones and anthropometric indicators of infants according to the type of feeding.

It has been accepted that satiety- and appetite-stimulating hormones play a role in the regulation of food intake and body composition during and after the lactation stage. Therefore, the purpose was to demonstrate that serum appetite-regulating hormones in infants differ according to anthropometric indicators and type of feeding. In a nonrandom cohort study, 169 mother-newborn dyads whose pregnancy and birth were attended at the Hospital Civil de Guadalajara were enrolled. According to the type of feeding, infants were classified as full breastfeeding (FBF), partial breastfeeding (PBF), and infants receiving human milk substitutes (HMS). Serum concentrations of ghrelin (pg/ml), leptin (ng/ml), peptide YY (pg/ml), and glucagon-like peptide-1 (GLP-1) (pM) were measured. Anthropometric measurements including weight, length, cephalic, arm circumference, tricipital, and subscapular skinfolds were obtained. Weight/age, weight/height, height/age, and BMI Z-score indexes were estimated. We performed one-way ANOVA, unpaired Student's t test, post hoc Tukey test, and Pearson correlation tests. The ANOVA comparison of the three feeding types showed significant differences in most anthropometric indicators (z-scores), especially between infants receiving FBF versus HMS and particularly on indicators of adiposity; no differences were observed in length and cephalic circumference z-scores at 8th and 16th weeks. Further, significant correlations were found between most of the adiposity indicators with ghrelin, leptin, and GLP-1, especially in infants who received FBF. There were differences in anthropometric and body composition parameters among infants receiving FBF, PBF, and HMS. There were significant correlations between body composition indicators with ghrelin, leptin, and GLP-1 mainly in infants receiving FBF.

Serum concentration of appetite-regulating hormones of mother-infant dyad according to the type of feeding.

Satiety and appetite-stimulating hormones play a role in the regulation of food intake. Breastfed infants may have a different profile of serum appetite-regulating hormones than formula-fed infants. We propose to demonstrate that the serum concentration of appetite regulatory hormones differs according to the type of feeding and that there is a correlation between the serum concentrations of these hormones in mothers and in infants at 4 months of age. In a cross-sectional analysis, 167 mother-newborn dyads at the Hospital Civil de Guadalajara were enrolled: 74 full breastfeeding (FBF), 56 partial breastfeeding (PBF), and 37 receiving human milk substitutes (HMS). Serum levels of ghrelin (pg/ml), leptin (ng/ml), peptide YY (pg/ml), and glucagon-like peptide-1 (GLP-1) (pM) were measured. We performed one-way analysis of variance, unpaired Student t test, post hoc Tukey test, and Pearson correlation. The total sample at 16 weeks postpartum included 167 dyads. The mean age was 16 ± 1 weeks. The concentrations of GLP-1 (pM) and peptide YY (pg/ml) were higher in the FBF group (42.6 and 442.9) than in the HMS group (35.2 and 401.9), respectively, p = 0.046 and p = 0.056. And, the FBF group had higher correlation coefficients of ghrelin (r = 0.411 vs. 0.165), GLP-1 (r = 0.576 vs. 0.407), and peptide YY (r = 0.218 vs. 0.067), respectively, than the HMS group. The concentrations of GLP-1 and peptide YY were higher in the FBF group when compared with the HMS group. Mother-infant dyads fed by FBF had more significant direct correlations of appetite-regulating hormones than those who received HMS.

BAFF-R and TACI expression on CD3+ T cells: Interplay among BAFF, APRIL and T helper cytokines profile in systemic lupus erythematosus.

BACKGROUND: Systemic lupus erythematosus (SLE) is the prototype of systemic autoimmune disease, characterized by loss of immune tolerance against self-antigens where autoantibody production is the hallmark of disease. B-cell-activating factor (BAFF) and A proliferation-inducing ligand (APRIL) are cytokines that promote autoreactive cell survival, immunoglobulin-class switching and autoantibody responses in human and mouse SLE models. BAFF and APRIL exert their functions through interactions with their receptors BAFF-R and TACI that are differentially expressed in B lymphocyte subsets, monocytes, dendritic cells and T lymphocytes. BAFF stimulation favors T lymphocyte activation and cytokine production through BAFF-R, which could contribute to the Th1, Th17 and/or Th2 response dysregulation observed in SLE patients. OBJECTIVE: To evaluate the expression of the cytokines BAFF and APRIL and their association with the receptors BAFF-R and TACI on CD3+ T cells and to evaluate Th1/Th2/Th17 cytokine profile in patients with SLE. METHODS: Fifteen healthy controls (HC) and 36 SLE patients were included, and their demographic and clinical data were assessed. The disease activity index (Mex-SLEDAI) and damage index (SLICC) were applied to the SLE patients. BAFF-R and TACI expression on CD3+ T cells were evaluated by flow cytometry. Serum BAFF and APRIL concentrations were measured by enzyme-linked immunosorbent assays (ELISA). Cytokine levels of Th1 (IL-12, IL-2, IFN-γ, TNF-α), Th2 (IL-4, IL-6, IL-10, IL-13) and Th17 (IL-1ß e IL-17) were quantified with a multiplex assay (MAGPIX). Statistical analysis was performed using PASW Statistics v.20 and GraphPad Prism v.6 software. RESULTS: No differences in BAFF-R or TACI expression on the CD3+ T cells of SLE and HC were observed. BAFF-R expression correlates inversely with disease activity (r = -0.538, p < 0.01), while TACI correlates with disease activity (r = 0.530, p < 0.05). Serum BAFF and APRIL levels were high in SLE patients and correlated with the disease activity index Mex-SLEDAI (r = 0.621, p < 0.01 and r = 0.416, p < 0.05). SLE patients were found to have significantly higher levels of IL-12, IFN-γ, TNF-α, IL-6, IL-10, IL-13, IL-1ß and IL-17 compared to HC (p < 0.05). Cytokines IL-17 (r = 0.526) and TNF-α (r = 0.410) correlate with disease activity (p < 0.05), while APRIL (r = 0.477), IL-10 (r = 0.426) and IFN-γ (r = 0.440) levels were associated with organ damage (p < 0.01). Serum BAFF expression levels correlate with IL-4 (r = 0.424; p < 0.05), IL-6 (r = 0.420; p < 0.05) and IL-10 (r = 0.459; p < 0.01), whereas APRIL levels correlate with IL-2 (r = 0.666; p < 0.01), IL-12 (r = 0.611; p < 0.01) and TNF-α (r = 0.471; p < 0.05) cytokines. A subgroup of SLE patients with high serum BAFF levels (>2 ng/mL) also showed increased APRIL, IL-2, IL-6 and IL-10 levels (p < 0.05). Finally, BAFF, IL-4 and TNF-α serum levels were associated with high titers of antinuclear antibodies. CONCLUSIONS: The study demonstrates an imbalance in the Th1/Th2 cytokine profile, with increased proinflammatory cytokines, as well as BAFF and APRIL serum levels. Associations of BAFF with Th2 profile cytokines and disease activity, as well as APRIL with Th1 profile cytokines and organ damage, suggest that BAFF and APRIL generated in the autoimmunity context could through still unknown mechanisms, modulate the microenvironment, and perpetuate the inflammatory response, autoantibody production and organ damage observed in SLE patients.