Effects of combined D-fagomine and omega-3 PUFAs on gut microbiota subpopulations and diabetes risk factors in rats fed a high-fat diet.
Mercè HereuSara Ramos-RomeroCristina BusquetsLidia Atienza-CuevasSusana AmézquetaBernat Miralles-PérezMaria Rosa NoguésLucía MéndezIsabel MedinaJosep Lluís TorresPublished in: Scientific reports (2019)
Food contains bioactive compounds that may prevent changes in gut microbiota associated with Westernized diets. The aim of this study is to explore the possible additive effects of D-fagomine and ω-3 PUFAs (EPA/DHA 1:1) on gut microbiota and related risk factors during early stages in the development of fat-induced pre-diabetes. Male Sprague Dawley (SD) rats were fed a standard diet, or a high-fat (HF) diet supplemented with D-fagomine, EPA/DHA 1:1, a combination of both, or neither, for 24 weeks. The variables measured were fasting glucose and glucose tolerance, plasma insulin, liver inflammation, fecal/cecal gut bacterial subgroups and short-chain fatty acids (SCFAs). The animals supplemented with D-fagomine alone and in combination with ω-3 PUFAs accumulated less fat than those in the non-supplemented HF group and those given only ω-3 PUFAs. The combined supplements attenuated the high-fat-induced incipient insulin resistance (IR), and liver inflammation, while increasing the cecal content, the Bacteroidetes:Firmicutes ratio and the populations of Bifidobacteriales. The functional effects of the combination of D-fagomine and EPA/DHA 1:1 against gut dysbiosis and the very early metabolic alterations induced by a high-fat diet are mainly those of D-fagomine complemented by the anti-inflammatory action of ω-3 PUFAs.
Keyphrases
- high fat diet
- insulin resistance
- fatty acid
- adipose tissue
- type diabetes
- risk factors
- glycemic control
- oxidative stress
- diabetic rats
- weight loss
- metabolic syndrome
- blood glucose
- cardiovascular disease
- skeletal muscle
- high glucose
- polycystic ovary syndrome
- physical activity
- anti inflammatory
- high fat diet induced
- drug induced
- heart failure
- acute heart failure
- endothelial cells
- climate change