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. 2014 Jul;9(4):406.
doi: 10.1007/s12263-014-0406-6. Epub 2014 May 20.

High-fat and obesogenic diets: current and future strategies to fight obesity and diabetes

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High-fat and obesogenic diets: current and future strategies to fight obesity and diabetes

João S Teodoro et al. Genes Nutr. 2014 Jul.

Abstract

Obesity, diabetes and their associated diseases are some of the greatest challenges that the world health care systems already face and with prospects of overburdening their capacities and funding. Due to decreased energetic expenditure and increased caloric intake, particularly in saturated fats, the number of people afflicted by said conditions is increasing by the day. Due to the failure, to this day, to effectively and ubiquity prevent and revert these diseases, the research into new compounds and therapeutic strategies is vital. In this review, we explain the most common dietary models of obesity and diabetes and the novel avenues of research we believe will be taken in the next few years in obesity and diabetes research. We primarily focus on the role of mitochondria and how the modulation of mitochondrial function and number as well as several promising therapeutic strategies involving metabolic regulators can positively affect the obese and diabetic status.

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Figures

Fig. 1
Fig. 1
Schematic representation of the convergence of pathways of the proposed therapeutic targets. The modulations of the activity of both AMPK and sirtuins (as, for example, the discussed Sirt1) lead to a potent activation of PGC-1α which, in turn, binds to an increase in the transcriptional activity of key target transcription factors. One example is PPARγ, a key transcription factor for metabolism. By acting on these targets, it is possible to elucidate molecular pathways and unveil therapeutic targets for exploration in the near future
Fig. 2
Fig. 2
The possibility of generating brown-like cells (“brite” adipocytes) from white adipocyte depots is an attractive therapeutic strategy, for these cells have an immense potential for energy consumption, rather than energy storage. As such, an isolated or combination therapy that can lead to the increase in “brite” cell content can cause a massive alteration of one’s metabolic status

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