Fasting and autophagy

The effect of fasting on autophagy induction Autophagy - the Novel Prize work by Japanese Researcher Dr. Ohsumi

Human being requires about 200 – 300 g of protein per day to live. On the other hand, human being takes only about 80 g of protein orally. The rest of protein is taken by cells through the process called autophagy, degradation and reutilization of unnecessary protein.

With this mechanism, the balance of synthesis and degradation of protein in our body is always kept constant. For example, human being can live about one month with only water, thanks to this mechanism.

In 2016, the Novel Prize in Physiology or Medicine was awarded to Japanese Researcher Dr. Yoshinori Ohsumi for elucidating the mechanisms underlying autophagy. Autophagy, a coined term meaning self-eating, is a “intracellular recycling system” that plays important roles in maintaining homeostasis and preventing nutritional, metabolic, and infection-mediated stresses.

Dr. Ohsumi was the world’s first to observe the autophagy through microscope using yeast cells under fasting conditions in 1988. He found that cytoplasmic components such as organelles and proteins are taken in by a particular organelle, the vacuole. He recalls, “It was an awe-inspiring sight that I could have kept watching for hours. For me, that was the breakthrough moment”.

Modulation of autophagy as a therapeutic target

Autophagy maintains normal cellular physiology to eliminate damaged organelles, long-lived misfolded proteins and invading pathogens, under stressful conditions, such as carcinogenic, infectious, degenerative, and deleterious agents. Thus, its dysregulation is shown to cause multiple human diseases. For example, neurodegenerative disorders such as Alzheimer’s, Parkinson’s, and Huntington’s diseases are triggered by the accumulation of abnormal protein resulting from disrupted autophagy in the nerve cells of the brain. As another example, fatty liver is shown to be related with the accumulation of protein called Rubicon, that suppresses autophagy. Thus, modulation of autophagy can be a potential therapeutic target for a diverse range of diseases, cancers and infectious diseases.

The effect of fasting by autophagy induction

Traditionally, fasting has been considered to have anti-aging effect. Since inhibition of autophagy pathway attenuates the anti-aging effects of fasting, it has been proposed that autophagy plays an important role in fasting and calorie restriction mediated anti-aging effect. Among several stress stimuli inducers of autophagy, fasting and calorie restriction are the most potent non-genetic autophagy stimulators. As a healthy practice, calorie restriction in the form of intermittent fasting in several clinical settings has been reported to promote several health benefits, including priming of immune response. Modulation of autophagy by intermittent fasting or calorie restriction is thus intensively investigated in the area including ischemia-reperfusion injury of the myocardium, prevention of COVID-19, and cancer treatment.

The effect of fasting on cancer therapy

The role of autophagy in cancer is complex, and its function may vary according to several biological factors, progression stage, and oncogene activation and inactivation. In this respect, autophagy can be related to either promotion or suppression of tumor growth and metastasis. Generally, cancer cells utilize autophagy for their metabolic needs even in hypoxic condition, thus inhibition of autophagy usually leads to induction of tumor cell death. However, to date, no clinical trials have demonstrated that inhibition of autophagy as a reliable therapeutic method for patients under cancer therapy. On the other hand, protocols targeting autophagy induction instead of autophagy blockade are under intense investigation in oncology.

Among those, intermittent fasting (alternate day fasting > 16hours) and calorie restriction (20-40%) are most investigated. Studies in in vivo and in vitro models have shown that intermittent fasting improved both chemotherapeutic response of many cytotoxic agents and radiologic sensitivity in models of most major cancers. Fasting in combination with cytotoxic agents is known to elicit differential response in normal and cancer cells, a phenomenon called differential stress resistance. When nutrients are absent, normal cells inactivate growth factor signaling while cancer cells don’t, thus becoming more vulnerable to cytotoxic treatment. Though the molecular mechanism of intermittent fasting has yet been cleared, in vitro data showed autophagy induction. The results of studies suggest that intermittent fasting can be applied to reduce side effects and toxicity in patients undergoing chemotherapy.













それらの中で、断続的断食(隔日断食> 16時間)とカロリー制限(20-40%)が最も研究されています。In vivoおよびin vitroモデルでの研究で、断続的絶食が多くの細胞毒性薬による化学療法反応、また多くの主要な癌モデルにおける放射線感受性の両方を改善したことが示されています。細胞毒性薬と組み合わせた絶食は、正常細胞と癌細胞で異なる反応を誘発することが知られており、これはストレス耐性格差と呼ばれる現象です。栄養素が存在しない場合、正常細胞は成長因子シグナル伝達を不活性化しますが、癌細胞はそうではないため、細胞毒性治療に対してより脆弱になります。断続的断食の分子メカニズムはまだ解明されていませんが、in vitroデータはオートファジー誘導を証明しました。研究の結果は、化学療法を受けている患者の副作用と毒性を減らすために断続的断食を適用できることを示唆しています。

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