Frailty syndrome is a medical condition that is characterised by a functional decline, usually from 65 years old on, and creates the need for assistance to perform daily living activities. As the population ages, the need for specialised geriatric care will increase immensely, and consequently, the need for specialised services for the care of these people will increase accordingly. From a nutritional point of view, to control or balance the nutritional status of residents will be essential in order to prevent sarcopenia and, consequently, frailty development. In this line, previous studies have highlighted the association among low energy intake, inadequate intake of protein and vitamin D, and an increased risk of frailty development. However, there is a lack of intervention studies on frail patients, especially in the realm of quality clinical trials. The few studies performed to date seem to indicate that there is a protective role of protein supplementation against frailty syndrome. In this regard, it is tempting to suggest daily 30 g protein supplements to prevent frailty. However, it is well established that excess protein can also be harmful; therefore, specific individual characteristics should be considered before prescribing these supplements. On the other hand, the relevance of other nutritional interventions, such as vitamin D, omega-3, and medium-chain triglycerides, is much more scarce in the literature. Therefore, we encourage the development of new clinical trials to carry out effective therapies to prevent frailty development.

To analyze in severely obese women the circadian expression of the clock genes hPer2, hBmal1, and hCry1 in explants from subcutaneous (SAT) and visceral (VAT) adipose tissue (AT), in order to elucidate whether this circadian clockwork can oscillate accurately and independently of the suprachiasmatic nucleus (SCN) and if glucocorticoid metabolism‐related genes such as glucocorticoid receptor (hGr) and 11β‐hydroxysteroid dehydrogenase 1 (h11βHsd1) and the transcription factor peroxisome proliferator activated receptor γ (hPPARγ) are part of the clock controlled genes. AT biopsies were obtained from morbid obese patients (BMI ≥40 kg/m²) (n = 7). Anthropometric variables were measured and fasting plasma lipids and lipoprotein concentrations were analyzed. In order to carry out rhythmic expression analysis, AT explants were cultured during 24 h and gene expression was performed at the following times (T): 0, 6, 12, and 18 h, with quantitative real‐time PCR. Clock genes oscillated accurately and independently of the SCN in AT explants. Their intrinsic oscillatory mechanism regulated the timing of other genes such as hPPARγ and glucocorticoid‐related genes. Circadian patterns differed between VAT and SAT. Correlation analyses between the genetic circadian oscillation and components of the metabolic syndrome (MetS) revealed that subjects with a higher sagittal diameter showed an increased circadian variability in hPer2 expression (r = 0.91; P = 0.031) and hBmal1 (r = 0.90; P = 0.040). Data demonstrate the presence of peripheral circadian oscillators in human AT independently of the central circadian control mechanism. This knowledge paves the way for a better understanding of the circadian contribution to medical conditions such as obesity and MetS.

Objective: To discuss present knowledge about adiponectin hormone.Design: Review of existing literature.Setting and results: Adiponectin is one of the most interesting cytokines associated with obesity, although its physiological role remains to be fully clarified. Adiponectin is a 247-amino acid protein that contains four differentiable domains. Contrary to most adipose-related cytokines, adiponectin levels are surprisingly lower in obese than in lean humans. Women have been found to have significantly higher adiponectin plasma concentrations than men. Further research is needed in order to identify new polymorphisms which contribute to explain the potential role of adiponectin in obesity and related pathologies.Considering the anti-inflammatory properties of adiponectin and the fact that it is negatively associated with adiposity, this cytokine could be one of the links between obesity and inflammation. The main mechanisms of action of adiponectin are directed to a protective role against atherogenic and insulin resistance processes. Research has revealed interesting new functions far beyond metabolism, such as immunity, cancer and bone formation.Contrary to all adipose-related proteins, adiponectin decreases with obesity. Most of the contradictory data surrounding adiponectin are related to plasma values and their relationship with body fat, gender differences and insulin resistance. There are important confounding results regarding the mechanisms of action and functions of adiponectin, especially in relation to insulin resistance and inflammation.