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Scope: Hypercholesterolemia increases the risk of mortality in type 2 diabetes mellitus (T2DM), especially in the late-stage. Consumption of bioactive compounds as functional ingredients would help achieve therapeutic goals for cholesterolemia. Silicon has demonstrated a hypocholesterolemic effect and the ability to reduce fat digestion. However, it is unclear whether silicon exerts such effect in late-stage T2DM (LD) and the intestinal mechanisms involved. Methods and results: Three groups of eight rats were included: early-stage T2DM control (ED), LD, and the LD group treated with silicon (LD-Si) once the rats were diabetic. Morphological alterations of the duodenal mucosa, and levels of markers involve in cholesterol absorption and excretion, beside cholesterolemia, and fecal excretion were assayed. Silicon included as a functional ingredient significantly reduces cholesterolemia in part due to: 1) reducing cholesterol intestinal absorption by decreasing the absorptive area and Acetyl-Coenzyme A acetyltransferase-2 (ACAT2) levels; and 2) increasing cholesterol excretion to the lumen by induction of the liver X receptor (LXR) and consequent increase of adenosine triphosphate-binding cassette transporter (ABCG5/8). Conclusions: These results provide insight into the intestinal molecular mechanisms by which silicon reduces cholesterolemia and highlights the efficacy of the consumption of silicon-enriched functional foods in late-stage T2DM.

This study explores the influence of carboxymethylcelullose (CMC) and methylcelullose (MC), added by simultaneous (sim) and sequential (seq) emulsification methods, on the structure, rheological parameters and in vitro lipid digestibility of pork lard O/W emulsions stabilized by soy protein concentrate (SPC). Five emulsions (SPC, SPC/CMC-sim, SPC/CMC-seq SPC/MC-sim, SPC/MC-seq) were prepared in vitro. The presence of CMC and MC, and the stage of incorporation affected the emulsion microstructure. In the SPC emulsion, lipid droplets were entrapped by a protein layer that was thicker when MC was added, providing greater resistance against environmental stresses during gastrointestinal digestion. At 37 °C, CMC incorporation produced a structural reinforcement of the SPC emulsion, whereas MC addition did not affect the network rigidity, although a delaying effect on the crossover temperature was observed, which was more evident in SPC/MC–seq. The presence and stage of CMC and MC incorporation affected the rate and extent of lipolysis, with SPC/MC-seq presenting an inferior concentration of free fatty acids. The lower extent of lipolysis observed in SPC/MC-seq may be positive in the manufacture of animal fat products in which reduced fatty acid absorption is intended.

The metabolic syndrome (MS) is a cluster of risk factors, such as central obesity, hyperglycemia, dyslipidemia, and arterial hypertension, which increase the probability of causing premature mortality. The consumption of high-fat diets (HFD) is a major driver of the rising incidence of MS. In fact, the altered interplay between HFD, microbiome, and the intestinal barrier is being considered as a possible origin of MS. Consumption of proanthocyanidins (PAs) has a beneficial effect against the metabolic disturbances in MS. However, there are no conclusive results in the literature about the efficacy of PAs in improving MS. This review allows a comprehensive validation of the diverse effects of the PAs on the intestinal dysfunction in HFD-induced MS, differentiating between preventive and therapeutic actions. Special emphasis is placed on the impact of PAs on the gut microbiota, providing a system to facilitate comparison between the studies. PAs can modulate the microbiome toward a healthy profile and strength barrier integrity. Nevertheless, to date, published clinical trials to verify preclinical findings are scarce. Finally, the preventive consumption of PAs in MS-associated dysbiosis and intestinal dysfunction induced by HFD seems more successful than the treatment strategy.