Role of Incretins in Muscle Functionality, Metabolism, and Body Composition in Breast Cancer: A Metabolic Approach to Understanding This Pathology.

A poorly studied issue in women with breast cancer is the role of incretins (GIP (glucose-dependent insulinotropic polypeptide) and GLP-1 (glucagon-like peptide-1)) in the quantity and quality of muscle mass in lean and obese individuals. The current report aims to analyze the patterns of association and the role of incretin in muscle functionality and body composition in women with cancer compared with healthy women (mammography BI-RADS I or II) to elucidate whether GIP and GLP-1 can be used to estimate the risk, in conjunction with overweight or obesity, for breast cancer. We designed a case-control study in women with a breast cancer diagnosis confirmed by biopsy in different clinical stages (CS; n = 87) and healthy women with a mastography BI-RADS I or II within the last year (n = 69). The women were grouped according to body mass index (BMI): lean (<25 kg/m2BS), overweight (≥25-<30 kg/m2BS), and obese (≥30 kg/m2BS). We found that GLP-1 and GIP levels over 18 pg/mL were associated with a risk of breast cancer (GIP OR = 36.5 and GLP-1 OR = 4.16, for the entire sample), particularly in obese women (GIP OR = 8.8 and GLP-1 OR = 6.5), and coincidentally with low muscle quality indexes, showed an association between obesity, cancer, incretin defects, and loss of muscle functionality.

Adipocytokines and Insulin Resistance: Their Role as Benign Breast Disease and Breast Cancer Risk Factors in a High-Prevalence Overweight-Obesity Group of Women over 40 Years Old.

Insulin levels, adipocytokines, and inflammatory mediators trigger benign breast disease (BBD) and breast cancer (BC). The relationship between serum adipocytokines levels, overweight-obesity, metabolic disturbs, and BC is unclear. Methods: To analyze the serum levels of the adipocytokines, insulin, and the HOMA IR in women without breast disease, with BBD or BC, and the role of these as risk factors for benign breast disease or breast cancer. Results: Adipsin values > 0.91 and visfatin levels > 1.18 ng/mL represent a risk factor to develop BBD in NBD lean women (OR = 18; and OR = 12). Data in overweight-obese women groups confirm the observation due to insulin levels > 2.6 mU/mL and HOMA IR > 0.78, with OR = 60.2 and 18, respectively; adipsin OR = 26.4, visfatin OR = 12. Breast cancer risk showed a similar behavior: Adipsin risk, adjusted by insulin and visfatin OR = 56 or HOMA IR and visfatin OR = 22.7. Conclusion: Adipose tissue is crucial for premalignant and malignant tissue transformation in women with overweight-obesity. The adipocyte−breast epithelium interaction could trigger a malignant transformation in a continuum, starting with BBD as premalignant disease, especially in overweight-obese women.

Breast benign disease and breast cancer risk. Overweight-obesity, biochemical, anthropometry. / Enfermedad mamaria benigna y riesgo de cáncer de mama: sobrepeso-obesidad, bioquímica, antropometría.

BACKGROUND: The immunologic, metabolic and anthropometric disturbances of overweight-obesity phenomena are risk factors to breast cancer (BC), particularly in proliferative benign breast disease women (PBBD). OBJECTIVE: To describe the adipocytokine levels, metabolic alteration and anthropometric characteristics in PBBD and its role as risk estimator to BC in a population with high overweight-obesity prevalence. MATERIAL AND METHODS: A cross-sectional study. We realized nutritional diagnosis, anthropometry, and we calculated the waist-height rate (WHR); serum measurement of adipocytokines, insulin and glucose and, HOMA IR determination in 27 PBBD and 27 BC women. We calculated mean, standard deviation, Pearson and Spearman correlation coefficients, Odds Ratio (OR) and confidence intervals through logistic regression as risk estimators of BC; p < 0.05 values were considered significant. RESULTS: Mean age in the PBBD group was minor than BC group, the humeral diameter was greater in BC group women. We did not find differences in anthropometry or adipocytokine levels; in both groups, the predominant somatotype was the endo-mesomorphic. We found higher insulin levels in BC group and a higher percentage of women with WHR > 0.5 too. The WHR > 0.5 + age over 50 were considered risk estimators to develop breast cancer in PBBD women group. CONCLUSION: The WHR >0.5 in women with PBBD over 50 years old could be considered an anthropometric risk estimator to develop BC.

INTRODUCCIÓN: La inflamación, las alteraciones metabólicas y antropométricas del fenómeno sobrepeso-obesidad son factores de riesgo para cáncer de mama (CaM) particularmente en mujeres con enfermedad mamaria benigna proliferativa (EMBP). OBJETIVO: Describir los niveles de adipocitocinas, alteraciones metabólicas y antropométricas en la EMBP y su papel como estimadores de riesgo para CaM en una población con prevalencia de sobrepeso-obesidad de más del 70%. MATERIAL Y MÉTODOS: Estudio transversal analítico en 27 mujeres con CaM y 27 con EMBP. Se realizó diagnóstico nutricional, antropometría y cálculo del índice cintura-talla (ICT); determinación sérica de adipocitocinas, insulina, glucosa y estimación de HOMA IR. Se calcularon promedio y desviaciones estándar, correlaciones de Pearson y Spearman; Odds Ratio (OR) e intervalos de confianza mediante regresión logística como estimadores de riesgo de CaM. Se consideró significativo un valor de p < 0.05. RESULTADOS: La edad del grupo EMBP fue menor. No se observaron diferencias en adipocitocinas ni antropometría (excepto el diámetro humeral fue mayor en CaM). Se observaron mayores niveles de insulina en CaM, y mayor porcentaje de mujeres con ICT > 0.5. El ICT > 0.5 + edad > 50 fueron estimadores de riesgo para CaM. CONCLUSIÓN: Un ICT > 0.5 en mujeres mayores de 50 años podría ser un estimador antropométrico de riesgo de CaM en mujeres con EMBP.

Relación entre índices de adiposidad visceral con componentes del síndrome metabólico en pacientes pediátricos con sobrepeso y obesidad / Relation among visceral adiposity index with components of metabolic syndrome in obese pediatric patients

Introducción: El síndrome metabólico (SM) consiste en conjunto de alteraciones metabólicas y cardiovasculares relacionadas con resistencia insulínica y la grasa visceral. Los índices antropométricos de adiposidad visceral son herramientas útiles que pudieran detectar complicaciones metabólicas en niños obesos. Objetivos: Determinar correlación entre índices de adiposidad visceral y componentes del SM en pacientes pediátricos obesos. Métodos: Estudio transversal, pacientes de 6-16 años. Inclusión: IMC ≥ 85p, exclusión: obesidad endógena, genopatías, uso de esteroides, silla de ruedas y yesos. Variables: CC (circunferencia de cintura), ICE (índice cintura-estatura), ICC (índice de cintura-cadera), TAS, TAD (tensión arterial sistólica y diastólica), triglicéridos, colesterol total, HDL (lipoproteína alta densidad), LDL (lipoproteína de baja densidad), VLDL (lipoproteína de muy baja densidad), ácido úrico sérico, insulina, índice de HOMA. Estándares internacionales para variables. Estadística: Frecuencias, porcentajes, medias/medianas, DS/rango, correlación Pearson. Resultados: 83 pacientes, mediana 11 años. 49 (51%) masculinos. Media IMC 31.4 (DS 6.3). Diagnóstico de obesidad visceral por ICE= 96.3%; por CC =80.7% y por ICC= 57.8%. Correlaciones: CC con TAS= r 0.35, p 0.001; TAD =r 0.29, p= 0.008; ácido úrico r =0.25, p 0.02 y con LDL-C = r 0.23, p 0.029. ICE con LDL r = 0.29, p 0.009. ICC con HDL r 0.34, p 0.002. Conclusiones: El ICE fue el que más detectó adiposidad visceral y el ICC fue el que menos diagnosticó. Las correlaciones significativas fueron: ICE con LDL; ICC con HDL y CC con TAS, TAD, LDL y ácido úrico sérico. La CC correlacionó con más componentes del SM (AU)

Metabolic syndrome (MS) consisting of set of metabolic and cardiovascular disorders related to insulin resistance and visceral fat. Anthropometric visceral adiposity indices are useful tools that could detect metabolic complications in obese children. Objective to determine correlation between visceral adiposity indices and components of MS in obese pediatric patients. Transversal, patients 6-16 years. Inclusion: BMI ≥ 85p, exclusion endogenous obesity, genopathies, steroid use, wheelchair and plasters. Variables: WC (waist circumference), WHtI (waist-height index), WHR (waist-hip ratio), SBP, DBP (systolic and diastolic blood pressure), triglycerides, total cholesterol, HDL (high lipoprotein density), LDL (low density lipoprotein) VLDL (very low-density lipoprotein), serum uric acid, insulin, HOMA index. international standards for variables. Statistics: frequencies, percentages, means / medium, DS / range, Pearson correlation. Results: 83 patients, median 11 years. 49 (51%) male. Average BMI 31.4 (SD 6.3). Diagnosis of visceral obesity = 96.3% by WHI; WC = 80.7% and 57.8% WHR. Correlations WC with SBP, r = 0.35, p 0.001; DBP, r = 0.29, p = 0.008; Uric acid r = 0.25, p 0.02 and LDL-C r= 0.23, p 0.029. WHI with LDL, r = 0.29, p 0.009. WHR with HDL, r 0.34, p 0.002. The WHtI was the most detected visceral adiposity and the WHR was the least diagnosed. We concluded the WC correlated with more components of MS. Significant correlations: WHtI with LDL; WHR with HDL and WC with SBP, DBP, LDL and serum uric acid (AU)

Reduction of the closure time of postoperative enterocutaneous fistulas with fibrin sealant.

AIM: To assess whether the use of fibrin sealant shortens the closure time of postoperative enterocutaneous fistulas (ECFs). METHODS: The prospective case-control study included 70 patients with postoperative ECFs with an output of < 500 mL/d, a fistulous tract of > 2 cm and without any local complication. They were divided into study (n = 23) and control groups (n = 47). Esophageal, gastric and colocutaneous fistulas were monitored under endoscopic visualization, which also allowed fibrin glue application directly through the external hole. Outcome variables included closure time, time to resume oral feeding and morbidity related to nutritional support. RESULTS: There were no differences in mean age, fistula output, and follow-up. Closure-time for all patients of the study group was 12.5 +/- 14.2 d and 32.5 +/- 17.9 d for the control group (P < 0.001), and morbidity related to nutritional support was 8.6% and 42.5%, respectively (P < 0.01). In patients with colonic fistulas, complete closure occurred 23.5 +/- 19.5 d after the first application of fibrin glue, and spontaneous closure was observed after 36.2 +/- 22.8 d in the control group (P = 0.36). Recurrences were observed in 2 patients because of residual disease. One patient of each group died during follow-up as a consequence of septic complications related to parenteral nutrition. CONCLUSION: Closure time was significantly reduced with the use of fibrin sealant, and oral feeding was resumed faster. We suggest the use of fibrin sealant for the management of stable enterocutaneous fistulas.

Contribution of TNF-308A and CCL2-2518A to carotid intima-media thickness in obese mexican children and adolescents.

BACKGROUND: Although commonly used in adults to detect early atherosclerosis, the value of the carotid intima-media thickness (CIMT) in children and adolescents is not clear. This marker has an inheritable component that supports the notion of a genetic influence. Among the genes studied as candidates for atherosclerosis development are those for chemokines, cytokines, and adhesion molecules because of their participation in atheroma formation through monocyte recruitment and migration. METHODS: We analyzed the relationship between CIMT and functional polymorphic variants in the genes for chemokines and proinflammatory cytokines associated with cardiovascular events in adults in lean and obese but otherwise healthy 6- to 19-year-old subjects. RESULTS: In the obese group, systolic blood pressure correlated negatively (r =-0.332; p = 0.008) and the TNF-308A allele correlated positively (r = 0.262; p = 0.040) with CIMT. The mean CIMT was higher in obese individuals with the TNF-308A allele than in those with TNF-308G allele (p = 0.041). In a multiple regression model for the total population, an increase in CIMT was explained by body mass index, systolic and diastolic blood pressure, and the TNF-308A and CCL2-2518A alleles (r(2) = 0.321; p = 0.022). CONCLUSIONS: This study contributes to the understanding of the pathophysiology of atherosclerosis and suggests that genetic markers of an increased inflammatory response and its deleterious effects are already present in obese children and adolescents.