Roberto Peromingo

Chronic Increase of Bone Turnover Markers After Biliopancreatic Diversion is Related to Secondary Hyperparathyroidism and Weight Loss. Relation with Bone Mineral Density

BackgroundBiliopancreatic diversion (BPD) is the most effective bariatric procedure. Around 70% of these patients have secondary hyperparathyroidism (SH) in the long term as a consequence of calcium and vitamin D malabsorption. This work was aimed to study the influence of SH on bone turnover and its relationship with bone mineral density (BMD).MethodsBone turnover markers were determined in 63 BPD patients and 34 morbidly obese controls. In the BPD group, we also studied the influence of age, loss of weight, common channel length, PTH, vitamin D, and serum calcium on bone turnover as well as its relation with BMD.ResultsBPD patients showed significantly higher PTH, osteocalcin, and β-CTx levels than controls. In the multivariate regression analysis, only PTH (β = 0.42; P = 0.0002), menopausal status (β = 0.31; P = 0.007) and the percentage of lost BMI (β = −0.24; P = 0.03) significantly predicted the osteocalcin level (R2 = 0.33; F = 9.56; P < 0.0001). Similarly, only PTH (β = 0.39; P = 0.0005), menopausal status (β = 0.37; P = 0.001) and the percentage of lost BMI (β = −0.23; P = 0.04) significantly predicted the β-CTx level (R2 = 0.33; F = 9.82; P < 0.0001). Osteocalcin and β-CTx levels correlated negatively with BMD at lumbar spine (r = −0.38, P = 0.002 and r = −0.30, P = 0.02, respectively).ConclusionsChronic SH and the loss of weight determine a high rate of bone turnover that is associated with decreasing BMD in BPD patients.

Retinol and α-Tocopherol in Morbid Obesity and Nonalcoholic Fatty Liver Disease

BackgroundWe aimed to study serum retinol and α-tocopherol in a cohort of obese patients and their possible association with several obesity-related conditions, given that the former may be implicated in a diminished capacity of anti-inflammatory and antioxidant potential in obese patients.MethodsEighty patients with morbid obesity participated in the study. Many clinical and biochemical variables were measured including serum retinol, α-tocopherol, aspartate aminotransferase (AST) and alanine aminotransferase (ALT) concentrations. Fatty liver was detected by ultrasonography.ResultsBoth serum retinol and α-tocopherol inversely correlated with body mass index (r = −0.334, P = 0.002 and r = −0.299, P = 0.007, respectively). Serum retinol inversely correlated with AST (r = −0.236, P = 0.036) and ALT (r = −0.241, P = 0.032). Multivariate regression analyses confirmed these results after correcting for the effects of other variables. Eighty-five percent of patients had fatty liver. When restricting the analysis to them, multivariate regression identified male sex (β = 0.451, P = 0.003), age (β = −0.275, P = 0.039), and serum retinol concentrations (β = −0.414, P = 0.005) as predictive variables on serum AST (R2 = 0.230, F = 3.408, P = 0.009) and male sex (β = 0.448, P = 0.003), age (β = −0.236, P = 0.046), insulin resistance determined by homeostasis model assessment (β = 0.243, P = 0.050), and serum retinol concentrations (β = −0.305, P = 0.022) as predictive variables on serum ALT (R2 = 0.296, F = 5.817, P = 0.001).ConclusionSerum retinol and α-tocopherol concentrations are inversely associated with body mass index in morbid obesity, and serum retinol is also inversely associated with serum concentrations of transaminases in those patients with nonalcoholic fatty liver disease.

Gene expression profiling of subcutaneous adipose tissue in morbid obesity using a focused microarray: Distinct expression of cell-cycle- and differentiation-related genes

BackgroundObesity results from an imbalance between food intake and energy expenditure, which leads to an excess of adipose tissue. The excess of adipose tissue and adipocyte dysfunction associated with obesity are linked to the abnormal regulation of adipogenesis. The objective of this study was to analyze the expression profile of cell-cycle- and lipid-metabolism-related genes of adipose tissue in morbid obesity.MethodsWe used a custom-made focused cDNA microarray to determine the adipose tissue mRNA expression profile. Gene expression of subcutaneous abdominal fat samples from 15 morbidly obese women was compared with subcutaneous fat samples from 10 nonobese control patients. The findings were validated in an independent population of 31 obese women and 9 obese men and in an animal model of obesity (Lepob/ob mice) by real-time RT-PCR.ResultsMicroarray analysis revealed that transcription factors that regulate the first stages of adipocyte differentiation, such as CCAAT/enhancer binding protein beta (C/EBPβ) and JUN, were upregulated in the adipose tissues of morbidly obese patients. The expression of peroxisome proliferator-activated receptor gamma (PPARγ), a transcription factor which controls lipid metabolism and the final steps of preadipocyte conversion into mature adipocytes, was downregulated. The expression of three cyclin-dependent kinase inhibitors that regulate clonal expansion and postmitotic growth arrest during adipocyte differentiation was also altered in obese subjects: p18 and p27 were downregulated, and p21 was upregulated. Angiopoietin-like 4 (ANGPTL4), which regulates angiogenesis, lipid and glucose metabolism and it is know to increase dramatically in the early stages of adipocyte differentiation, was upregulated. The expression of C/EBPβ, p18, p21, JUN, and ANGPTL4 presented similar alterations in subcutaneous adipose tissue of Lepob/ob mice.ConclusionsOur microarray gene profiling study revealed that the expression of genes involved in adipogenesis is profoundly altered in the subcutaneous adipose tissue of morbidly obese subjects. This expression pattern is consistent with an immature adipocyte phenotype that could reflect the expansion of the adipose tissue during obesity.