Abstract:Financiación. Los datos de este análisis proceden del estudio ENRICA, que fue financiado por Sanofi-Aventis. La financiación específica para este análisis procede de los proyectos FIS PI13/02321 y "Cátedra UAM de Epidemiología y Control del Riesgo Cardiovascular", Madrid, España. Este estudio está dirigido por un comité científico independiente.Conflicto de intereses. M. Teresa Aguilera es empleada de Sanofi-Aventis. No obstante, esta empresa no comercializa ningún producto relacionado con leptina u obesidad.
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“…This is consistent with the condition of insulin resistance observed in the present study. Leptin was also elevated in these subjects with overweight/obesity; although no reference values have been internationally established, the concentrations obtained here were above the cut-off values for cardiometabolic abnormalities reported in a Spanish sample of 11,000 subjects, i.e, 6.45 ng/mL for males and 23.75 ng/mL for females (Gijón-Conde et al, 2015). Nevertheless, this increase in leptin concentration was not related to any iron marker value.…”
Background
Controversy exists on the relationship between iron metabolism and cardiometabolic risk. The aim of this study was to determine if there is a link between dysmetabolic iron and cardiometabolic markers in subjects with excess body weight.
Methods
Cross-sectional study with fifty participants presenting overweight or obesity and at least another metabolic syndrome factor. Determinations: anthropometry, body composition, blood pressure, lipids, glucose, insulin, leptin, areas under the curve (AUC) for glucose and insulin after an oral glucose tolerance test, hs-C reactive protein (hs-CRP), blood count, ferritin, transferrin, transferrin saturation (TSAT), soluble transferrin receptor (sTfR). Gender-adjusted linear correlations and two independent samples t tests were used.
Results
Ferritin was positively correlated with insulin-AUC (r = 0.547, p = 0.008) and TSAT was negatively correlated with waist-hip ratio (r = − 0.385, p = 0.008), insulin (r = − 0.551, p < 0.001), and insulin resistance (HOMA-IR, r = − 0.586, p < 0.001). Subjects with TSAT ≤ 20% had higher insulin (p = 0.012) and HOMA-IR (p = 0.003) compared to those with TSAT > 20%. In conclusion, the observed results suggest that iron transport and storage are altered in subjects with overweight/obesity, at the same time that they exhibit the characteristic features of insulin resistance. Nevertheless, this occurs without iron overload or deficiency. These results should be validated in wider cohorts since they suggest that iron transport and storage should be assessed when performing the clinical evaluation of subjects with excess body weight.
“…This is consistent with the condition of insulin resistance observed in the present study. Leptin was also elevated in these subjects with overweight/obesity; although no reference values have been internationally established, the concentrations obtained here were above the cut-off values for cardiometabolic abnormalities reported in a Spanish sample of 11,000 subjects, i.e, 6.45 ng/mL for males and 23.75 ng/mL for females (Gijón-Conde et al, 2015). Nevertheless, this increase in leptin concentration was not related to any iron marker value.…”
Background
Controversy exists on the relationship between iron metabolism and cardiometabolic risk. The aim of this study was to determine if there is a link between dysmetabolic iron and cardiometabolic markers in subjects with excess body weight.
Methods
Cross-sectional study with fifty participants presenting overweight or obesity and at least another metabolic syndrome factor. Determinations: anthropometry, body composition, blood pressure, lipids, glucose, insulin, leptin, areas under the curve (AUC) for glucose and insulin after an oral glucose tolerance test, hs-C reactive protein (hs-CRP), blood count, ferritin, transferrin, transferrin saturation (TSAT), soluble transferrin receptor (sTfR). Gender-adjusted linear correlations and two independent samples t tests were used.
Results
Ferritin was positively correlated with insulin-AUC (r = 0.547, p = 0.008) and TSAT was negatively correlated with waist-hip ratio (r = − 0.385, p = 0.008), insulin (r = − 0.551, p < 0.001), and insulin resistance (HOMA-IR, r = − 0.586, p < 0.001). Subjects with TSAT ≤ 20% had higher insulin (p = 0.012) and HOMA-IR (p = 0.003) compared to those with TSAT > 20%. In conclusion, the observed results suggest that iron transport and storage are altered in subjects with overweight/obesity, at the same time that they exhibit the characteristic features of insulin resistance. Nevertheless, this occurs without iron overload or deficiency. These results should be validated in wider cohorts since they suggest that iron transport and storage should be assessed when performing the clinical evaluation of subjects with excess body weight.
“…Sus niveles séricos reflejan la cantidad de energía depositada en él; por lo tanto, son proporcionales a la cantidad de grasa corporal, así los adipocitos de mayor tamaño producen mayor cantidad de leptina. Es así como la leptina, además de actuar como una señal de saciedad, actúa como una señal de adiposidad y sus niveles séricos tienen una alta correlación con el IMC y el PGC en humanos y en animales (7)(8)(9)19).…”
Section: Discussionunclassified
“…Sus niveles se encuentran elevados en la mayoría de los humanos obesos, debido a sus mayores porcentajes de grasa corporal y al desarrollo de resistencia a su acción. Personas con deficiencia de leptina, probablemente, representan una minoría de humanos obesos (7)(8)(9).…”
Antecedentes: la obesidad es un factor de riesgo para las enfermedades crónicas no transmisibles. Objetivo: explorar la relación entre indicadores antropométricos y niveles de leptina en un grupo de madres y en sus hijos. Materiales y métodos: estudio transversal en 74 binomios madre-hijo de Cali, Colombia. Se realizó caracterización sociodemográfica, evaluaciones antropométricas y leptina sérica en 56 madres y 26 niños. Se usaron coeficientes de correlación entre los indicadores antropométricos y la leptina. Resultados: las madres presentaron 35,5 % de exceso de peso, elevada grasa corporal en un 80 % y niveles de leptina de 20,5 ng/mL. Los niños tenían 20,7±2,4 meses de edad; 8,2 % de exceso de peso; 4,1 % desnutrición aguda y niveles de leptina de 1,85 ng/mL. En madres e hijos las correlaciones entre indicadores antropométricos fueron significativas y positivas, lo mismo con leptina en las madres, pero en los niños solo correlacionó débilmente con peso/talla e IMC-edad. La leptina en las madres se correlacionó débilmente con indicadores antropométricos de los niños, pero no al contrario. Conclusión: la prevalencia de exceso de peso es alta en las madres y menor en los niños. La leptina en las madres se correlaciona débilmente con indicadores antropométricos de los niños, pero no al contrario.
“…Relevant phenotypic information is summarized in Additional file 2 : Table S1 [ 31 – 40 ]. Anthropometric magnitudes were measured under standardized methods.…”
Background
Overweight and obesity are defined by an anomalous or excessive fat accumulation that may compromise health. To find single-nucleotide polymorphisms (SNPs) influencing metabolic phenotypes associated with the obesity state, we analyze multiple anthropometric and clinical parameters in a cohort of 790 healthy volunteers and study potential associations with 48 manually curated SNPs, in metabolic genes functionally associated with the mechanistic target of rapamycin (mTOR) pathway.
Results
We identify and validate rs2291007 within a conserved region in the 3′UTR of folliculin-interacting protein FNIP2 that correlates with multiple leanness parameters. The T-to-C variant represents the major allele in Europeans and disrupts an ancestral target sequence of the miRNA miR-181b-5p, thus resulting in increased FNIP2 mRNA levels in cancer cell lines and in peripheral blood from carriers of the C allele. Because the miRNA binding site is conserved across vertebrates, we engineered the T-to-C substitution in the endogenous Fnip2 allele in mice. Primary cells derived from Fnip2 C/C mice show increased mRNA stability, and more importantly, Fnip2 C/C mice replicate the decreased adiposity and increased leanness observed in human volunteers. Finally, expression levels of FNIP2 in both human samples and mice negatively associate with leanness parameters, and moreover, are the most important contributor in a multifactorial model of body mass index prediction.
Conclusions
We propose that rs2291007 influences human leanness through an evolutionarily conserved modulation of FNIP2 mRNA levels.
Graphical Abstract
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