Just trudging on with exams, got one tonight and my last one on Thursday- in the home stretch! I’ve also got some really exciting plans post-exams including giving a lecture to a group of high schoolers on metabolism, homeostasis, nutrition etc… am really looking forward to it . I’m also excited for a Christmas party my roommate and I are throwing this Friday, and of course excited to a) deck our house out with Christmas decorations and b) make Christmas goodies.

Here’s a pic of me climbing earlier this year

So with the holiday season approaching, I figured I’d do a post on a common holiday problem: overeating. Hope you enjoy

The following will be a description of what should normally happen in a normal sized meal. As we eat, sugar and fat get pushed through our metabolic pathways and create substrates for our Electron Transport Chain (ETC) at the mitochondrial membranes of our cells. The ETC can take those substrates and, by passing electrons through a series of complexes, create energy in the form of ATP. That energy is then transported out of the mitochondria (via the ANT and phosphocreatine shuttle) so that the energy will then be available to our muscles. This is a pretty (maybe overly) simplified description of what happens during the metabolism of fat and sugar for fuel.
So with a little back ground information…

What happens after we binge? When we eat in excess, more substrates become available to the ETC- more than the ETC can handle; a back pressure will be created and the passing of the electrons from complex to complex will be slowed. Ions will spend more time at each complex and have a greater chance to combine with oxygen to form superoxide; more reactive oxygen species will be created. The ROS created, although it has a bad rep from a cancer perspective, serves a purpose in the cell to adjust the ETC to a healthier speed (and in turn result in less ROS produced).

So how does ROS help us then? In order to adjust the ETC to a more suited speed, a lower energy environment (i.e. more ADP: ATP) is required. The ROS inactivates a few enzymes in previous metabolic pathways and results in an increased storage of our fuel in fat (triglycerides), which also (via MalCoA) inactivates fat transporters that bring fat into the mitochondria for metabolism by the ETC. Less substrate will be available to the ETC and the speed will be able to adjust. Triglycerides are the normal and healthy way we should be storing fat. Take home point- one binge won’t kill you… the trouble comes from chronic binging.

Following a westernised diet with regular bouts of excessive calories, the concentrations of triglycerides are much higher; the path to create triglycerides will become saturated and less efficient. The inefficient production of triglycerides will result in more fatty acid intermediates in our cells which are where the big problems lie. The fat intermediates inhibit normal insulin signalling, the ANT at the ETC (leading to more ROS) and also MalCoA’s (from the pathway to store energy in the form of triglycerides) ability to block fat uptake by the mitochondria. Take home point- chronically overeating leads to chronically higher levels of ROS created from the ETC. If we want to protect ourselves from excessive ROS production from the ETC, our bodies need to divert fat and sugar away from the mitochondria. We can decrease the ROS from the ETC by either exercise (increased turnover) or smaller caloric intakes (less substrates).

So on a more macro level… fat is the first insult from chronically binging; we will have a harder time storing fat properly. Less subcutaneous (which is protective) and more visceral (pro-inflammatory) fat may eventually result. As fat cells increase in size, their vasculature decreases leading to hypoxia and then inflammation and macrophage recruitment. These fat cells will end up releasing both cytokines (which promote inflammation) and excess fatty acids (which promote an unhealthy fat distribution and toxicity to other tissues). Insulin resistance will soon also occur in the fat cells.

I could write a book about the negative effects from binge eating, but for the sake of keeping this (relatively) brief- I’ll end here. It’s easy to fall into a trap of constantly overeating, which is pretty well the norm in North America. One binge leads to two and so on and so forth. Hopefully this gives some of you guys more incentive towards sticking to a healthy diet, especially with Christmas around the corner.

Wish me luck on tonight’s exam!

Jen

Dulloo AG, Montani JP. (2012) Body composition, inflammation and thermogenesis in pathways to obesity and the metabolic syndrome: an overview. Obes Rev. Suppl 2:1-5. doi: 10.1111/j.1467-789X.2012.01032.x.

Fantino M. (2011)Role of lipids in the control of food intake. Curr Opin Clin Nutr Metab Care. (2):138-44. doi: 10.1097/MCO.0b013e3283437b78.

Kassab A, Piwowar A. (2012) Cell oxidant stress delivery and cell dysfunction onset in type 2 diabetes. Biochimie.:1837-48. doi: 10.1016/j.biochi.2012.01.020.

Martínez JA. (2006)Mitochondrial oxidative stress and inflammation: an slalom to obesity and insulin resistance. J Physiol Biochem.:303-6.

Medina-Gómez G. (2012) Mitochondria and endocrine function of adipose tissue. Best Pract Res Clin Endocrinol Metab.:791-804. doi: 10.1016/j.beem.2012.06.002.