Gut Microbiota, Metabolic Disorders and Breast Cancer: Could Berberine Turn Out to Be a Transversal Nutraceutical Tool? A Narrative Analysis

Abstract

Metabolic disorders, mainly characterized as the marked alteration of the lipid and carbohydrate profile, in addition to the clinical presence of the direct consequences of these alterations, are pathological conditions that have considerably increased in prevalence in recent years. They are directly linked to the onset of various pathologies, including cancer, particularly breast cancer, and are hormone-responsive. Alongside the known conditions responsible for this scenario, such as nutrition and lifestyle in general, the importance of both the colonic microbiota and the various organs and systems is becoming increasingly evident. In fact, it is now evident that microbial dysbiosis plays a fundamental role in the onset of these metabolic disorders, and therefore how these conditions are indirectly responsible for the onset and progression of neoplasms. Indirect mechanisms such as an altered Firmicutes/Bacteroidetes ratio; the formation of metabolites such as short-chain fatty acids (SCFAs), in particular, butyrate, which is capable of acting as a tumor suppressor; and the glucuronidase activity of estroboloma (bacteria responsible for estrogen metabolism) are just some of the most important mechanisms that contribute to the history of breast cancer. It is therefore understandable that in clinical terms, it is essential to associate the modulation of metabolic disorders and the microbial conditions that contribute to generating them with common therapies, preferably using compounds and solutions that are effective and acceptable for the patient without side effects. Nutraceuticals such as berberine (active both in metabolic scenarios and in the microbiota) and interventions modulating the microbial structure such as the use of probiotics and prebiotics seem to be ideal solutions for these preventive and no-longer-ignorable strategies in the light of numerous data now present in the literature.

Clostridium butyricum Strain MIYAIRI 588 (CBM588) as a Precision Probiotic Therapy in the Ketogenic Diet: A Possible Application?

“…For berberine, in addition to documented anti-inflammatory effects, the ability (similarly to Boswellia) to favor the reduction in the Firmicutes/Bacteroides ratio, a functional factor for a good response to the ketogenic diet, is also described. Furthermore, berberine, by favoring the development of Akkermansia muciniphila, acts synergistically with CMB588 in promoting mucus production and colonic epithelial barrier integrity [96,97]. Anti-inflammatory/senolytic effects are also described for quercetin [98,99], but above all, prebiotics are functional to the reduction in the Firmicutes/Bacteroides ratio in animal models of non-alcoholic fatty liver disease (NFLD) [100].…”

Sports-Related Gastrointestinal Disorders: From the Microbiota to the Possible Role of Nutraceuticals, a Narrative Analysis

“…thrive in the colon and terminal ileum after BBR treatment, populations of Ruminococcus gnavus, Ruminococcus schinkii, Lactobacillus acidophilus, Lactobacillus murinus, and Lactococcus lactis decrease. Some studies indicate that berberine can increase levels of Akkermansia muciniphila in the intestinal microbiota [103,109,[111][112][113][114]. BBR also modulates immune cell activity, suppressing the expression of inflammatory factors such as interleukin (IL)-1β, IL-4, IL-10, and tumor necrosis factor (TNF)-α, thereby mitigating low-grade inflammation.…”

Novel Anti-Cancer Products Targeting AMPK: Natural Herbal Medicine against Breast Cancer

“…To date, the study of the effects of berberine on breast cancer cells has not conclusively determined the regulatory role of berberine in relation to AMPK. Some research has examined the potent effects of gut microbiota and metabolic constituents [ 206 ]. In HepG2 hepatoma cells and liver tissues in high-fat-fed mice, berberine attenuated triglyceride accumulation by activating AMPK and in turn decreased the expression of SREBP-1c and stearyl-coenzyme A desaturase 1 (SCD1) [ 207 ].…”