Modulation of mitochondrial function with the Mediterranean diet

Researchers have examined current understanding regarding the Mediterranean diet (MedDiet) and the function of mitochondria with regard to health consequences in a study that was published in the Experimental Gerontology Journal.

The role that subcellular organelles known as mitochondria play in numerous energy processes is well understood. A rising corpus of studies demonstrates that mitochondria play a crucial part in the body’s reaction to short-term and long-term stress exposure.

Interest in these organelles is increased by this biological reaction to adversity in terms of psychological and physical functioning in a number of disorders typical in older persons.

Furthermore, MedDiet also seems to affect mitochondrial activity, which supports its involvement in lowering the risk of negative health impacts.

Polyphenols and the MedDiet
There is considerable evidence supporting MedDiet’s abundance in polyphenols and other naturally occurring compounds with potent antioxidant properties, as well as its power to scavenge free radicals and regulate endogenous antioxidant defense mechanisms.

The mitochondrial antioxidant enzymes may contribute to these effects. Polyphenols help reduce inflammation and mitochondrial dysfunction linked to metabolic syndrome because of their antioxidant properties. (MetS).

Additionally, the antioxidant properties of the MedDiet polyphenols improved mitochondrial damage and apoptosis and decreased the production of mitochondrial reactive oxygen species (mtROS) in a number of experimental studies. Numerous studies have found that MedDiet’s high fiber content has positive effects on health.

The benefits of diets rich in polyphenols on MetS, which mediates mitochondrial control, have been examined in several in vitro investigations.

Using human endothelial cells as an atherosclerosis cellular model, chlorogenic acid (CGA) in apples and coffee beans was evaluated for its protective benefits against ox-low-density lipoprotein (LDL)-induced endothelial cell dysfunction.

CGA demonstrated mitochondria-mediated effects by increasing the activity of the silent mating-type information regulation 2 homolog-1 (SIRT1) and up-regulating the adenosine monophosphate-activated protein kinase (AMPK) and peroxisome proliferator-activated receptor-gamma coactivator (PGC)-1 messenger ribonucleic acid (mRNA) to sustain mitochondrial biogenesis.

Additionally, CGA therapy reduced the production of ROS by endothelial cells, which had an effect on cytoprotection.

MedDiet contains delphinidin
In endothelial cells with vascular endothelial growth factor (VEGF)-induced mitochondrial dysfunction, delphinidin was found to counteract the elevated levels of mitochondrial respiration, mt-deoxyribonucleic acid (DNA), and complex IV activity.

Delphinidin also increased the expression of transcription factors such as DNA polymerase gamma (PolG), nuclear-related factor 1 (NRF1), transcription factor B2 of the mitochondria (TFB2m), and transcription factor A of the mitochondria (TFAm).

Each of these proteins plays a part in the regulation of mitochondrial biogenesis. In mice exposed to lipopolysaccharide, lycopene (LYC), a phytochemical from the carotenoid family found in tomatoes and grapefruits, reduced mitochondrial dysfunction and inflammation.

LYC enhanced the tissue mRNA levels of SIRT1, PGC1, cyclooxygenase 5b (Cox5b), cyclooxygenase 8b (Cox8b), cyclooxygenase 7a1 (Cox7al), and cytochrome c.

The MedDiet’s resveratrol and whole carbs
Whole carbs are another significant dietary category in MedDiet that benefits metabolic diseases.

In order to protect against H2O2-induced oxidative stress found in rat pheochromocytoma, the Sirtuin 3-Forkhead box O3a (SIRT3-FOXO3a) signaling system is particularly activated by 5-heptadecylresorcinol, a biomarker for ingestion of whole grain rye.

By preserving mitochondrial respiration and membrane potential while reducing ROS levels in the mitochondria, it also boosted adenosine triphosphate (ATP) generation and cell metabolism.

Other studies have demonstrated that the antioxidant properties of resveratrol, which is found in foods including grapes, berries, and chocolate, vary on the individual’s age and dose.

When it comes to improving the function of a solubilized mitochondrial complex, this polyphenol competes with nicotinamide. Another example of the prebiotic resveratrol properties that alter the diversity and composition of the gut microbiota is the lowered Firmicutes/Bacteroidetes ratio, which is instead raised in obese people and patients with systemic disorders.

Resveratrol administration reduces the formation of trimethylamine-N-oxide (TMAO), a byproduct of carnitine and choline. A high quantity of TMAO is considered a risk factor for heart attack and stroke because it promotes platelet activity and predisposes to thrombosis.

fatty acids in short chains and metabolism
Short-chain fatty acids are the byproduct of the gut microbiota’s fermentation of insoluble fiber. (SCFAs). There is evidence that SCFAs can control a number of metabolic illnesses, such as type 2 diabetes, insulin intolerance, and obesity.

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Butyrate, an SCFA present in the MedDiet, promotes fatty acid metabolism and boosts mitochondrial function. The nuts, vegetables, and shellfish in MedDiet include significant amounts of polyunsaturated fatty acids (PUFAs). The consumption of PUFAs is widely established to reduce the risk of developing cardiometabolic disorders.

Numerous human studies have demonstrated the MedDiet’s bioactive components’ beneficial effects on MetS, demonstrating enhanced health advantages by focusing on mitochondria.

This approach may provide additional pharmacological and nutritional benefits, notably for the gastrointestinal system and muscular strength.

According to the study’s findings, high-quality meals like MedDiet are associated with lower levels of oxidative stress and, as a result, a lower incidence of diseases.

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Future intervention studies are needed to better understand how the MedDiet impacts mitochondrial activity and to highlight the role of these cells in the pathophysiology of illnesses that affect elderly people often.


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