Abstract
Sweeteners have become integrating components of the typical western diet, in response to the spreading of sugar-related pathologies (diabetes, obesity and metabolic syndrome) that have stemmed from the adoption of unbalanced dietary habits. Sweet proteins are a relatively unstudied class of sweet compounds that could serve as innovative sweeteners, but their introduction on the food market has been delayed by some factors, among which is the lack of thorough metabolic and toxicological studies. We have tried to shed light on the potential of a sweet protein, MNEI, as a fructose substitute in beverages in a typical western diet, by studying the metabolic consequences of its consumption on a Wistar rat model of high fat diet-induced obesity. In particular, we investigated the lipid profile, insulin sensitivity and other indicators of metabolic syndrome. We also evaluated systemic inflammation and potential colon damage. MNEI consumption rescued the metabolic derangement elicited by the intake of fructose, namely insulin resistance, altered plasma lipid profile, colon inflammation and translocation of lipopolysaccharides from the gut lumen into the circulatory system. We concluded that MNEI could represent a valid alternative to fructose, particularly when concomitant metabolic disorders such as diabetes and/or glucose intolerance are present.
Highlights
The major changes in dietary habits observed over the past decades, with the ready availability of sugars and processed food, have led, both in wealthy and developing countries, to an increase in metabolism-related diseases
high fat plus fructose (HFF) translated group consumed more energy intakewater, from beverages, butfructose our results show that this induced compensatory reductionofofthirst the sweetened because consumption is known toastimulate the sensation calories introduced via high fat diet, as expected since it is known that the rat rodent model possesses
By considering the central role of tumor necrosis factor α (TNF-α) in obesity-induced insulin resistance in peripheral organs [26], we hypothesized an involvement of this cytokine in the onset of insulin resistance in HFF rats, but we found no variations of TNF-α levels between all the groups of rats in skeletal muscle and in TNF-inducible transcription factor NFkB p65, a pathway normally antagonizing insulin signaling [28]
Summary
The major changes in dietary habits observed over the past decades, with the ready availability of sugars and processed food, have led, both in wealthy and developing countries, to an increase in metabolism-related diseases. In response to this trend, natural and artificial sweeteners have been massively introduced in the food and beverage market as sugar substitutes. Harmful effects of the consumption of artificial sweeteners on the gut microflora, with consequences on glucose tolerance, have emerged [2] Even sweeteners such as fructose are not devoid of risks: we have demonstrated that a fructose-rich diet induces metabolic syndrome, inflammation and oxidative stress in a rat model of obesity [3,4]. A relatively unexplored class of sweet compounds is constituted by Sweet Proteins (SPs), which were first isolated
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