Mitochondria diabetes and cancer

Mitochondria diabetes and cancer

or 'cancerous cell love sugar, what better recommendation can you have?'

How and why do ‘normal’ somatic cells go rogue and become cancers? So much is known of the ‘how’ and in such mind-boggling detail one would have thought that some ‘motive’ would have been uncovered by now.

Of course I don’t really mean to imply  higher levels of heretical motivation to single cells going about their daily tasks as part of a multicellular collective,  or do I?  No-one after all would be embarrassed to speculate as to why say an amoeba did something or another. They might say “ this behaviour is an adaptive response to a chemical diffusing in its environment’ as it duly swims away exhibiting what they would term negative-chemotaxis.

Cells in a multicellular organism could equally  do what they will but they normally don’t. They don’t because:

a) They are physically prevented from moving being as they are part of tissues like liver, muscle kidney and so on.

b)They have stopped dividing, these  are called post-mitotic cells and form the bulk of a multicellular creature’s body like our own.

Cancers rarely form  from cells in these situations, however cells near the outer boundaries of tissues or which form part of the circulating cells ( in blood or lymph) are much more likely to rebel ... being both able to divide and even move. So most cancers are from dividing tissues ( skins or epithelia as called eg: the skin lining the outer shell, the gut, mouth, gullet, womb, cervix, lung, breast ) and mobile tissues ( blood cancers , testicular, ovarian).

More rarely, much more rarely, cells deep within tissues rebel; the common cancers above are called carcinomas the latter sarcomas. Whatever, it looks like opportunity is as always an important factor in transgression from virtue to rogue. Sticking with this the theme of opportunity. What metabolic cue can provide even more opportunity?  I think the answer is sugar. Here’s why.

It is well known that the eukaryote cell is a chimera, albeit an ancient and well integrated one between an anaerobic host and the aerobic symbiont the bacteria-like  mitochondrion.
Biochemically the putative host’s  metabolism is  sugar processing  and the mitochondrion is able to take the host’s sugar waste products as well as their own normal fatty foods and fully oxidise them liberating a lot of energy, enough indeed to build a big complex multicellular creature like us. This is the orthodoxy of student biochemistry, glycolysis followed by oxidative phosphorylation.

Mitochondria are the accidental ‘guests’ that make the miracle of the modern cell.
But, at the end of the day, bacterial-like invasion of a cell,  no matter how ‘beneficial’, is an invasion to be fought … given the opportunity. It is well documented that cancer cells suppress mitochondria, preventing them from dividing and respiring. Sugar metabolism is enough for cancers to get by and divide, albeit normally very slowly. But why suppress mitochondria? Surely more energy is a bonus if you want to grow quickly? The obvious answer is that this is personal. They want mitochondria gone.

It is now also becoming well known that Type 2 diabetes is strongly associated with cancer.
Unsurprisingly,  diabetic and more significantly perhaps pre-diabetic  conditions are associated with elevated blood glucose levels. Technically I mean elevated fasting glucose levels, that is higher than normal blood sugar when not actually eating sugar. This in my opinion is nothing less than adding another opportunity for a cell ‘wanting’ to return to its origins.

To add motivation to opportunity, how would one eject invaders from your cell? There is no real way to do this directly … but, if you divide repeatedly, and have already prevented the 'invader' from reproducing, then some cells will become free from the infection ...  applying the simple maths of dilution.

In short, cancer could be a defence albeit atavistic in the extreme to the invasion of the host cell by mitochondria. This reaction is effectively and normally comprehensively suppressed in a  multicellular organism and any opportunistic rogue cells  are ruthlessly destroyed by the marauding defensive immune-police.

But what about tipping the balance? Rapidly dividing cells in a sugary environment might just have enough opportunities lined up for one or two to be successful rogue 'start-ups'.

If then time reduces  immune surveillance through old age or stress  then  the ancient 'saccharophile' gts its chance to fight back.