{"id":3224,"date":"2020-07-28T00:00:00","date_gmt":"2020-07-27T22:00:00","guid":{"rendered":"https:\/\/www.neolifesalud.com\/breast-cancer-and-insulin\/"},"modified":"2023-01-06T17:43:48","modified_gmt":"2023-01-06T16:43:48","slug":"breast-cancer-and-insulin","status":"publish","type":"post","link":"https:\/\/www.neolifesalud.com\/en\/blog\/prevention-and-anti-aging\/breast-cancer-and-insulin\/","title":{"rendered":"Breast cancer and insulin"},"content":{"rendered":"
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The increase of adiposity after menopause has been associated with an increased risk of breast cancer. In truth, one of the keys may lie in hyperinsulinism.<\/strong><\/h1>\n

Diabetes\/insulin resistance and breast cancer are pathologies that are quite different but the route of insulin has a central, common role in both. By identifying this metabolic alteration, we will be able to act using our best weapons: diet, exercise, and metformin.<\/p>\n

Dr. Celia Gonzalo Gleyzes – Neolife Medical Team<\/em><\/p>\n

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About insulin<\/strong><\/p>\n

Insulin<\/strong> is a peptide hormone<\/strong> produced by the beta cells of the pancreas when there is an increase of plasma glucose (in the blood).<\/p>\n

This hormone<\/strong> stimulates glucose uptake by the muscles and adipose tissue. In the liver, insulin inhibits gluconeogenesis (the formation of glucose) and the release of glucose.<\/p>\n

\"Breast<\/p>\n

High levels of glucose<\/strong> make the liver and the muscles store the excess glucose.<\/p>\n

In the adipocytes, insulin promotes the transport of fatty acids in the bloodstream, their storage (lipogenesis), and it inhibits lipolysis. Summing up, insulin<\/strong> facilitates the storage of energy so that it can be mobilized when the levels of insulin are low (fasting).<\/p>\n

Apart from the aforementioned organs, insulin<\/strong> also has effects on the neurons, the endothelial cells (cells that line the blood vessels), and immune cells.<\/p>\n

To avoid getting lost in the different concepts, we\u2019re going to briefly review the route of insulin.<\/p>\n

Insulin<\/strong> attaches to the insulin receptor and activates cellular signaling pathways that are key regulators of cellular homeostasis<\/strong>. These signaling pathways are altered in the majority of biologically aggressive cancers.<\/p>\n

Under circumstances rich in nutrients, insulin<\/strong> is released and attaches to the insulin receptor. This binding of insulin promotes tyrosine phosphorylation of the insulin receptor and the insulin receptor substrate (IRS). The IRS, in turn, phosphorylates phosphatidylinositol-3-kinase (PI3K) and activates signaling of the AKT\/mTOR pathway.<\/p>\n

Insulin also activates signaling of insulin\/IGF-1. IGF-1 binds to its receptor, leading to phosphorylation cascades that activate the PI3K\/AKT\/mTOR pathway and the ras\/RAF\/mitogen-activated protein kinase<\/em> (MAPK).<\/p>\n

Insulin resistance<\/strong><\/p>\n

Overeating alters the balance between energy storage and energy consumption, leading the individual to prediabetes <\/strong>(insulin resistance<\/strong>) and later to type 2 diabetes <\/strong> mellitus<\/strong>. Having high levels of insulin because of that overeating brings about desensitization of the skeletal muscle. The pancreas is forced to produce insulin continuously and these beta cells will eventually die (the stage in which the person with type 2 diabetes mellitus will require insulin).
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Hyperinsulinism in the liver causes dyslipidemia (increased LDL cholesterol and triglycerides) and favors the development of fatty liver<\/strong> (hepatic steatosis).<\/p>\n

In the brain, a sustained increase in insulin<\/strong> stimulates appetite, favoring weight gain. In the skeletal muscle, hyperinsulinism and insulin resistance make the muscle unable to take advantage of glucose<\/strong>; thus, the person affected will have less tolerance to physical exercise<\/strong> and also general tiredness.<\/p>\n

In adipose tissue, hyperinsulinism increases lipid accumulation and causes inflammation.<\/p>\n

In blood vessels and the kidney, insulin promotes<\/strong>endothelial cell damage and renal dysfunction due to increased nitric oxide synthesis, increased reactive oxygen species, and decreased cell adhesion.<\/p>\n

Insulin and cancer<\/strong><\/p>\n

Below, we will note the mechanisms that relate hyperinsulinism<\/strong> and tumorigenesis<\/strong>:<\/p>\n