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Incluso se te permite darte algunos caprichillos sin que eso suponga recuperar todo lo perdido hasta el momento como pasa en algunas otras dietas. Todo esto que puede parecer algo complicado y pesado por lo de las cantidades, os aseguro que te acostumbras enseguida. En primer lugar, las visitas dependen mucho de la dietista que te toque ya que hay alguna francamente regular y poco motivadora. Pero lo peor es que una vez que has alcanzado tu peso ideal y te ponen en fase de mantenimiento tienes que seguir "pasando por caja" simplemente por pesarte y aunque no asistas a las reuniones. Y la verdad que no he engordado desde que la hago. Como muchas verduras y lo que necesito son recetas nuevas, estoy cansada.

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The contents of this supplement are solely the responsibility of the authors and do not necessarily represent official views of the IUNS. The supplement coordinators had no conflicts of interest to disclose. Summa and F. Turek, no conflicts of interest. E-mail: ude. Abstract Recent advances in the understanding of the molecular, genetic, neural, and physiologic basis for the generation and organization of circadian clocks in mammals have revealed profound bidirectional interactions between the circadian clock system and pathways critical for the regulation of metabolism and energy balance.

The discovery that mice harboring a mutation in the core circadian gene circadian locomotor output cycles kaput Clock develop obesity and evidence of the metabolic syndrome represented a seminal moment for the field, clearly establishing a link between circadian rhythms, energy balance, and metabolism at the genetic level.

Dietary nutrients have been shown to influence circadian rhythms at both molecular and behavioral levels; and many nuclear hormone receptors, which bind nutrients as well as other circulating ligands, have been observed to exhibit robust circadian rhythms of expression in peripheral metabolic tissues. Furthermore, the daily timing of food intake has itself been shown to affect body weight regulation in mammals, likely through, at least in part, regulation of the temporal expression patterns of metabolic genes.

Taken together, these and other related findings have transformed our understanding of the important role of time, on a h scale, in the complex physiologic processes of energy balance and coordinated regulation of metabolism.

This research has implications for human metabolic disease and may provide unique and novel insights into the development of new therapeutic strategies to control and combat the epidemic of obesity. These rhythms are generated and sustained by a genetically encoded molecular pacemaker i.

This circadian clock system enables organisms to preferentially sequester reactions, pathways, and behaviors to particular times to optimize functioning and increase fitness. For example, cyanobacteria, single-celled organisms that derive energy from the sun, can use their circadian clock to synthesize, assemble, and activate the photosynthetic machinery immediately before sunrise to maximize energy harvest during the day.

Later in the day, the clock can direct the deactivation of photosynthesis to avoid inefficiency and energy wasting during darkness. Recent studies have revealed the profound interactions between the circadian clock system and energy regulation and metabolism at many levels of organization, which have substantial implications for human metabolic diseases, such as obesity and diabetes.

This review summarizes key experimental findings linking the circadian clock to energy balance and metabolism in mice, beginning with the initial description of the development of obesity and metabolic syndrome in mice harboring a mutation in the core circadian gene circadian locomotor output cycles kaput Clock 4. This genetic linkage between the core molecular oscillator and metabolic function has contributed to a growing interest in the relations between circadian rhythms and metabolism at biochemical and molecular levels, which has led to a number of important discoveries and advances in understanding the role of the circadian clock and its complex, bidirectional interactions with critical metabolic pathways.

Next, the role of nutrient composition of the diet on circadian rhythms is discussed, as well as the finding that many nutrient- and dietary ligand—binding nuclear hormone receptors in peripheral metabolic organs exhibit robust diurnal and circadian patterns of expression, potentially representing part of the interface linking diet and the circadian clock. In addition to dietary composition, the timing of food intake has recently emerged as an important factor mediating body weight regulation and the organization of metabolism in mice.

Finally, evidence from clinical, observational, and epidemiologic studies in humans is presented, along with a discussion of the implications of the findings in mice for human health and metabolic disease, with particular emphasis on obesity.

Current Status of Knowledge Genetic link between the clock and metabolism. However, these studies remain complicated by a variety of other unhealthy behaviors that are common in shift workers, such as poor diet, lack of physical activity, and insufficient sleep. Therefore, the description of the first genetic evidence linking the circadian clock system to energy regulation and metabolism provided a critical step forward for the field, enabling a flurry of biochemical, genetic, molecular, and physiologic studies capable of addressing the underlying mechanisms and pathways.

In the initial report, mice harboring a mutation in the core circadian gene Clock termed Clock mutant mice were fed a high-fat HF diet and observed to develop obesity at a young age, as well as a variety of metabolic and endocrine abnormalities consistent with the metabolic syndrome 2. The Clock mutants were also shown to exhibit reduced overall expression levels and a blunted diurnal rhythm of orexin mRNA, a hypothalamic neuropeptide involved in energy regulation 2.

Taken together, these results indicate profound metabolic dysfunction and energy imbalance in these mice that have a genetically defective circadian clock. A striking feature of the metabolic phenotype of the Clock mutant mice was the presence of hyperglycemia and hypoinsulinemia, a pattern suggestive of a defect along the insulin axis 2. Furthermore, mice lacking a functional circadian clock in the pancreatic islets were shown to develop frank diabetes at an early age due to insufficient insulin secretion 3.

These mice were genetically engineered to eliminate the circadian clock machinery from the pancreatic islets alone, leaving normal clock function in remaining tissues intact. These results illustrate an important aspect of the circadian clock system: it acts cell-autonomously and exhibits specific functions limited to particular cell types and tissues. Those functions differ depending on the tissue, enabling the clock to regulate biologic processes in a tissue-specific manner, dependent on the needs of the individual tissue.

For example, the clock in the liver has been shown to play a critical role in regulating blood glucose concentrations during feeding and fasting cycles throughout the diurnal cycle 4. At the level of the entire organism, these tissue-specific functions are coordinated temporally by the master circadian clock in the hypothalamic suprachiasmatic nucleus SCN , which entrains to the solar cycle and synchronizes cellular clocks throughout the body 5.

Through this regulatory role, the circadian clock mediates the temporal patterns of the downstream effects of SIRT1 8 , 9 , establishing an additional link between the clock and cellular metabolism. Through coordinated patterns of chromatin modification, the clock was then shown to regulate oscillations in metabolic gene expression 10 , particularly in the liver. This process enables the liver to properly regulate energy metabolism: disruption of the rhythmic binding and deacetylation by HDAC3 leads to excessive fat accumulation in hepatocytes, resulting in hepatic steatosis In human populations, genome-wide association studies have revealed associations between variants of the circadian clock—related gene Mntr1b, which encodes melatonin receptor 1B, fasting glucose concentrations, and the risk of type 2 diabetes 12 — The pineal hormone melatonin is synthesized and released with a robust daily oscillation that is regulated by the master circadian clock in the SCN and ambient light exposure Variants in the core circadian clock gene Crytochrome 2 Cry2 have also been recently associated with fasting glucose concentrations and type 2 diabetes risk 17 , These results provide additional evidence, from human populations, for a genetic relation between the circadian clock system and metabolic function and the risk of metabolic diseases.

Together, these findings, as well as a number of others, have helped usher in a revolution in understanding the relations between circadian rhythms, metabolism, and energy balance at the biochemical, genetic, and molecular levels.

In addition, they harkened back to a previous finding that the DNA binding activity of components of the core circadian clock machinery, CLOCK and BMAL1 which together form a heterodimer , is regulated by redox state 19 , suggesting that metabolic flux within the cell is capable of interacting with, and potentially regulating, the circadian clock. Interestingly, more recent studies have described a highly conserved circadian rhythm in the oxidation of peroxiredoxin proteins, which persists in the absence of transcription 20 — 22 , raising intriguing questions related to the connections and relations between metabolic cycles and circadian rhythms within cells, as well as the evolutionary origins of the circadian clock itself.

Dietary impacts on circadian rhythms. Although there has been a tremendous amount of interest in the role of the clock in regulating biochemical pathways and metabolic processes, relatively less effort has been expended examining how metabolic inputs themselves affect the clock. In an early study addressing this question, wild-type mice with a genetically intact circadian pacemaker were fed an HF diet and monitored carefully to determine how the properties of the circadian clock system were affected The free-running period of the clock i.

The robust effect on period length was observed after only 2 wk of feeding the diet and persisted for several weeks afterward. Finally, concentrations of circulating metabolic markers and the expression of circadian clock and metabolic genes were disrupted by the HF diet, typically leading to blunted rhythms Taken together, these results demonstrate that an HF diet is capable of affecting circadian rhythms at both behavioral and molecular levels, suggesting that metabolic inputs can influence the functioning of the clock.

One possibility is that certain nutritional components of the HF diet act through specific receptors to influence the circadian clock, although this hypothesis was not tested directly in the experiment.

The mechanism s of the effects of the HF diet on the clock remains unknown, so additional studies are necessary to elucidate the specific impacts of dietary components on the circadian clock and its properties.

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