Obesity is a serious medical condition worldwide, which needs new approaches and recognized international consensus in treating diseases leading to morbidity. The aim of this review was to examine heterogeneous links among the various phenotypes of obesity in adults. Proteins and associated genes in each group were analysed to differentiate between biomarkers. A variety of terms for classification and characterization within this pathology are currently in use; however, there is no clear consensus in terminology. The most significant groups reviewed include metabolically healthy obese, metabolically abnormal obese, metabolically abnormal, normal weight and sarcopenic obese. These phenotypes do not define particular genotypes or epigenetic gene regulation, or proteins related to inflammation. There are many other genes linked to obesity, though the value of screening all of those for diagnosis has low predictive results, as there are no significant biomarkers. It is important to establish a consensus in the terminology used and the characteristics attributed to obesity subtypes. The identification of specific molecular biomarkers is also required for better diagnosis in subtypes of obesity.

We present the pressure area isotherms for Langmuir films made of calix[8]arene, the calix[8]arene/C60 complex, and the calix[8]arene/C70 complex, all of them measured at 306.1 K. A Brewster angle microscope was used to observe the phases shown by the π−A isotherms. In these three cases, we found a solid phase and its solid−gas coexistence but no expanded liquid phases. The Langmuir films made of calix[8]arene and the calix[8]arene/C60 complex are very similar. The experimental information is consistent with the assumption that C60 is situated inside the cavity of calix[8]arene. The Langmuir films of calix[8]arene and the calix[8]arene/C70 complex are not very similar; we present a discussion to explain the origin of this difference.

Mammalian class I aldehyde dehydrogenase (ALDH) plays an important role in the biosynthesis of the hormone retinoic acid (RA), which modulates gene expression and cell differentiation. RA has been shown to mediate control of human ALDH1 gene expression through modulation of the retinoic acid receptor α (RARα) and the CCAAT/enhancer binding protein β (C/EBPβ). The positive activation of these transcription factors on the ALDH1 promoter is inhibited by RA through a decrease of C/EBPβ binding to the ALDH1 CCAAT box response element. However, the mechanism of this effect remains unknown. Here we report that the RARα/retinoid X receptor β (RXRβ) complex binds to the mouse retinaldehyde dehydrogenase 1 (Raldh1) promoter at a non-consensus RA response element (RARE) with similar affinity to that of the consensus RARE. We found that C/EBPβ binds to a Raldh1 CCAAT box located at -82/-58 bp, adjacent to the RARE. Treatment with RA increases GADD153 and GADD153-C/EBPβ interaction resulting in a decreased cellular availability of C/ EBPβ for binding to the Raldh1 CCAAT box. These data support a model in which high RA levels inhibit Raldh1 gene expression by sequestering C/EBPβ through its interaction to GADD153.

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