Epigenetics, 1-Carbon Metabolism, and Homocysteine During Dysbiosis.

Although a high-fat diet (HFD) induces gut dysbiosis and cardiovascular system remodeling, the precise mechanism is unclear. We hypothesize that HFD instigates dysbiosis and cardiac muscle remodeling by inducing matrix metalloproteinases (MMPs), which leads to an increase in white adipose tissue, and treatment with lactobacillus (a ketone body donor from lactate; the substrate for the mitochondria) reverses dysbiosis-induced cardiac injury, in part, by increasing lipolysis (PGC-1α, and UCP1) and adipose tissue browning and decreasing lipogenesis. To test this hypothesis, we used wild type (WT) mice fed with HFD for 16 weeks with/without a probiotic (PB) in water.

Diet-induced chronic syndrome, metabolically transformed trimethylamine-N-oxide, and the cardiovascular functions.

Recent studies have shown that the integrity of the gastrointestinal tract and its microbiome impact the functioning of various body systems by regulating immunological responses, extracting energy, remodeling intestinal epithelia, and strengthening the gut itself. The gastrointestinal tract microbiota includes bacteria, fungi, protozoa, viruses, and archaea which collectively comprise a dynamic community prone to alterations via influences such as the environment, illness, and metabolic processes. The idea that the host's diet possesses characteristics that could potentially alter microbiota composition is a novel notion.

Dysbiotic 1-carbon metabolism in cardiac muscle remodeling.

Unless there is a genetic defect/mutation/deletion in a gene, the causation of a given disease is chronic dysregulation of gut metabolism. Most of the time, if not always, starts within the gut; that is what we eat. Recent research shows that the imbalance between good versus bad microbial population, especially in the gut, causes systemic diseases.