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1
Food Preferences and Obesity

Sara Spinelli,Erminio Monteleone 대한내분비학회 2021 Endocrinology and metabolism Vol.36 No.2
Obesity is a multifactorial disease with several potential causes that remain incompletely understood. Recent changes in the environment, which has become increasingly obesogenic, have been found to interact with individual factors. Evidence of the role of tasteresponsiveness and food preference in obesity has been reported, pointing to a lower taste sensitivity and a higher preference and intake of fat and, to a lesser extent, sweet foods in obese people. Studies in the last decades have also suggested that individual differences in the neurophysiology of food reward may lead to overeating, contributing to obesity. However, further studies are needed toconfirm these findings. In fact, only a limited number of studies has been conducted on large samples, and several studies were conducted only on women. Larger balanced studies in terms of sex/gender and age are required in order to control the confounding effect of these variables. As many factors are intertwined in obesity, a multidisciplinary approach is needed. This will allow a betterunderstanding of taste alteration and food behaviours in obese people in order to design more effective strategies to promote healthier eating and to prevent obesity and the related chronic disease risks.
2
Sensory Science for New Healthy and Palatable Tailor-Made Meal Solutions for Individuals Suffering from Taste Alterations

Sara Spinelli 한국식품영양과학회 2022 한국식품영양과학회 학술대회발표집 Vol.2022 No.10
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3
Recurrent ETNK1 mutations in atypical chronic myeloid leukemia

Gambacorti-Passerini, Carlo B.,Donadoni, Carla,Parmiani, Andrea,Pirola, Alessandra,Redaelli, Sara,Signore, Giovanni,Piazza, Vincenzo,Malcovati, Luca,Fontana, Diletta,Spinelli, Roberta,Magistroni, Vera American Society of Hematology 2015 Blood Vol.125 No.3
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Despite the recent identification of recurrent SETBP1 mutations in atypical chronic myeloid leukemia (aCML), a complete description of the somatic lesions responsible for the onset of this disorder is still lacking. To find additional somatic abnormalities in aCML, we performed whole-exome sequencing on 15 aCML cases. In 2 cases (13.3%), we identified somatic missense mutations in the ETNK1 gene. Targeted resequencing on 515 hematological clonal disorders revealed the presence of ETNK1 variants in 6 (8.8%) of 68 aCML and 2 (2.6%) of 77 chronic myelomonocytic leukemia samples. These mutations clustered in a small region of the kinase domain, encoding for H243Y and N244S (1/8 H243Y; 7/8 N244S). They were all heterozygous and present in the dominant clone. The intracellular phosphoethanolamine/phosphocholine ratio was, on average, 5.2-fold lower in ETNK1-mutated samples (P < .05). Similar results were obtained using myeloid TF1 cells transduced with ETNK1 wild type, ETNK1-N244S, and ETNK1-H243Y, where the intracellular phosphoethanolamine/phosphocholine ratio was significantly lower in ETNK1-N244S (0.76 ± 0.07) and ETNK1-H243Y (0.37 ± 0.02) than in ETNK1-WT (1.37 ± 0.32; P = .01 and P = .0008, respectively), suggesting that ETNK1 mutations may inhibit the catalytic activity of the enzyme. In summary, our study shows for the first time the evidence of recurrent somatic ETNK1 mutations in the context of myeloproliferative/myelodysplastic disorders.