6 research outputs found

    You are what you eat, or are you? The challenges of translating high-fat-fed rodents to human obesity and diabetes

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    Obesity and type 2 diabetes mellitus (T2DM) are rapidly growing worldwide epidemics with major health consequences. Various human-based studies have confirmed that both genetic and environmental factors (particularly high-caloric diets and sedentary lifestyle) greatly contribute to human T2DM. Interactions between obesity, insulin resistance and ÎČ-cell dysfunction result in human T2DM, but the mechanisms regulating the interplay among these impairments remain unclear. Rodent models of high-fat diet (HFD)-induced obesity have been used widely to study human obesity and T2DM. With >9000 publications on PubMed over the past decade alone, many aspects of rodent T2DM have been elucidated; however, correlation to human obesity/diabetes remains poor. This review investigates the reasons for this translational discrepancy by critically evaluating rodent HFD models. Dietary modification in rodents appears to have limited translatable benefit for understanding and treating human obesity and diabetes due—at least in part—to divergent dietary compositions, species/strain and gender variability, inconsistent disease penetrance, severity and duration and lack of resemblance to human obesogenic pathophysiology. Therefore future research efforts dedicated to acquiring translationally relevant data—specifically human data, rather than findings based on rodent studies—would accelerate our understanding of disease mechanisms and development of therapeutics for human obesity/T2DM

    The human gut microbiome and its role in obesity and the metabolic syndrome

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    The gut microbiota helps balance key vital functions for the host, including immunity and nutritional status. Studies have also linked the microbiome to human mood and behavior, as well as many gut disorders, eczema, and a number of systemic disorders (Azad et al., CMAJ 185:385–394, 2013). Changes in the gut microbiota composition and/or activity may be implicated in the control of inflammation, fat storage, and altered glucose response in obese patients. Dietary short-chain fatty acids appear to be “indirect nutrients” produced by the gut microbiota that can modulate adiposity and immunity as well as send signals to the gut to produce hormones that regulate appetite, permeability, and inflammation. Numerous data have been published regarding differences in the composition of the gut microbiota in obesity. Taken together, the data currently published suggest that specific changes in the gut microbiota occur in overweight or obese patients and are either positively or negatively linked with adiposity, inflammation, and glucose or lipid homeostasis. Manipulation of the microbiota though diet can promote healthy weight loss by altering gut function and metabolism. Probiotics and prebiotics are interesting research tools to assess the relevance of specific bacteria in obesity. Prebiotics may lessen obesity and related metabolic stress by modulating gut peptides involved in the control of appetite and gut barrier function

    SEIS: Insight’s Seismic Experiment for Internal Structure of Mars

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