ArticlePDF Available

Abstract

[This corrects the article DOI: 10.1155/2011/269043.].
Corrigendum
Corrigendum to “Sequence Analysis of the UCP1 Gene in a Severe
Obese Population from Southern Italy”
Giuseppe Labruna ,
1
Fabrizio Pasanisi,
2
Giuliana Fortunato,
3
,
4
Carmela Nardelli ,
3
,
4
Carmine Finelli ,
5
Eduardo Farinaro ,
6
Franco Contaldo,
2
and Lucia Sacchetti
3
,
4
1
Fondazione IRCCS SDN, Istituto di Ricerca Diagnostica e Nucleare, Via Gianturco 113, 80143 Naples, Italy
2
Centro Interuniversitario di Studi e Ricerche sull’Obesit`
ae Dipartimento di Medicina Clinica e Sperimentale,
Universit`
adegli Studi di Napoli Federico II, Via Pansini 5, 80131 Naples, Italy
3
CEINGE Biotecnologie Avanzate S.C. a R.L., Via Gaetano Salvatore 486, 80145 Naples, Italy
4
Dipartimento di Biochimica e Biotecnologie Mediche, Universit`
adegli Studi di Napoli Federico II, Via Pansini 5,
80131 Naples, Italy
5
Independent Researcher, Naples, Italy
6
Dipartimento di Scienze Mediche Preventive, Universit`a degli Studi di Napoli Federico II, Via Pansini 5, 80131 Naples, Italy
Correspondence should be addressed to Lucia Sacchetti; sacchett@unina.it
Received 19 May 2018; Accepted 28 May 2018; Published 19 July 2018
Copyright ©2018 Giuseppe Labruna et al. is is an open access article distributed under the Creative Commons Attribution
License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is
properly cited.
In the article titled “Sequence Analysis of the UCP1 Gene in
a Severe Obese Population from Southern Italy” [1], the fifth
author, Carmine Finelli, is not affiliated to the Fondazione Stella
Maris Mediterraneo and should be listed as an independent
researcher. e corrected list of affiliations is shown above.
References
[1] G. Labruna, F. Pasanisi, G. Fortunato et al., “Sequence analysis
of the UCP1 gene in a severe obese population from southern
Italy,” Journal of Obesity, vol. 2011, Article ID 269043, 4 pages,
2011.
Hindawi
Journal of Obesity
Volume 2018, Article ID 3260210, 1 page
https://doi.org/10.1155/2018/3260210
... Microorganisms 2020, 8, 485 2 of 13 of obese individuals (~14%), as measured by body mass index (BMI) > 30 kg/m 2 (Data from https: //www.epicentro.iss.it/passi/dati/sovrappeso). Except for rare forms of monogenic obesity, common obesity is a multifactorial disorder whose onset genetics, epigenetics, behavioral and environmental aspects contribute, from prenatal to adulthood [2][3][4][5][6][7]. A further factor likely to be involved in the insurgence of obesity is represented by the gut microbiota [8,9]. ...
Article
Full-text available
The gut microbiota may have an impact on obesity. To date, the majority of studies in obese patients reported microbiota composition in stool samples. The aim of this study was to investigate the duodenal mucosa dysbiosis in adult obese individuals from Campania, a region in Italy with a very high percentage of obese people, to highlight microbial taxa likely associated with obesity. Duodenum biopsies were taken during upper gastrointestinal endoscopy in 19 obese (OB) and 16 lean control subjects (CO) and microbiome studied by 16S rRNA gene sequencing. Duodenal microbiome in our groups consisted of six phyla: Proteobacteria, Firmicutes, Actinobacteria, Fusobacteria, Bacteroidetes and Acidobacteria. Proteobacteria (51.1% vs. 40.1%) and Firmicutes (33.6% vs. 44.9%) were significantly (p < 0.05) more and less abundant in OB compared with CO, respectively. Oribacterium asaccharolyticum, Atopobium parvulum and Fusobacterium nucleatum were reduced (p < 0.01) and Pseudomonadales were increased (p < 0.05) in OB compared with CO. Receiver operating characteristic curve analysis showed Atopobium and Oribacterium genera able to discriminate with accuracy (power = 75% and 78%, respectively) OB from CO. In conclusion, increased Proteobacteria and decreased Firmicutes (Lachnospiraceae) characterized the duodenal microbiome of obese subjects. These data direct to further studies to evaluate the functional role of the dysbiotic-obese-associated signature.
Article
Full-text available
Brown adipose tissue, where Uncoupling Protein 1 (UCP1) activity uncouples mitochondrial respiration, is an important site of facultative energy expenditure. This tissue may normally function to prevent obesity. Our aim was to investigate by sequence analysis the presence of UCP1 gene variations that may be associated with obesity. We studied 100 severe obese adults (BMI > 40 kg/m(2)) and 100 normal-weight control subjects (BMI range = 19-24.9 kg/m(2)). We identified 7 variations in the promoter region, 4 in the intronic region and 4 in the exonic region. Globally, 72% of obese patients bore UCP1 polymorphisms. Among UCP1 variants, g.IVS4-208T>G SNP was associated with obesity (OR: 1.77; 95% CI = 1.26-2.50; P = .001). Further, obese patients bearing the g.-451C>T (CT+TT) or the g.940G>A (GA+AA) genotypes showed a higher BMI than not polymorphic obese patients (P = .008 and P = .043, resp.). In conclusion, UCP1 SNPs could represent "thrifty" factors that promote energy storage in prone subjects.