Hey! I was wondering how detailed an answer you wanted. Other replies have indicated environmental effectors such as sports and diet as regulators of fat accumulation, but not how they bring about such effects. There are multiple levels of molecular events that lead to different capacities to accumulate fat, but I will focus on one particular one that I think underpins regulation of all the others, and could use more attention.
When we talk about energy and metabolism, we have to talk about mitochondria. No escaping it. However, I will not tell you that mitochondria are the “powerhouse of the cell”, as it paints them into a static role. To the contrary, mitochondria are highly dynamic organelles involved in cellular senescence (permanent arrest of cell division), apoptosis, and inflammation (http://journals.plos.org/plosbio…
Most people have been instructed in high school biology that calories are translated from energy in food to cellular energy using the mitochondria. This is true in the case of carbohydrates, fatty acids, and proteins, where they are pre-processed by the cell, then fed into the mitochondria as “acetyl-CoA” in tandem with a reductive (in context of redox) cofactor called NADH, to produce ATP. (2NADH + 2ADP + 2Pi + O2–> 2 ATP + H2O)
This process happens via oxidative phosphorylation, where NADH donates an electron (e-) into the electron transport chain (ETC) as well as a hydrogen ion (H+) into the mitochondrial intermembrane space (Figure 1). Crucially, the larger concentration of H+ on the outer side of the membrane vs the inner side sets up a chemiosmotic gradient across the membrane. Think of it like a dam through which hydrogen ions flow and generate energy. Because the ions are charged, there is also an electrical potential across the membrane, equivalent to 100-140 mV at normal levels.
Figure 1. In the process of finding this figure, I found out that it has been used by another Quoran previously. It’s such a nice and succinct figure. (The renaissance of mitochondrial pH), (Why is the inner mitochondrial membrane impermeable to H+
The electron transport chain is formed of four or five protein complexes that pass these electrons on sequentially from one complex to the next. The final protein complex is called ATP synthase. Here, hydrogen ions flow from the outside of the membrane inwards, from high to low concentration, where they are paired back up with the electrons and coupled with oxygen molecules to produce H2O. This reaction drives ATP production.
So why have you told me this?
Well, see figure 1. There is a membrane protein on the left called UCP. Its full name is Uncoupling Protein. UCPs, especially UCP1, promote leakage of H+ ions from the outer side of the membrane into the inside, relieving some of the membrane potential. In addition, the decreased concentration of hydrogen ions means that there is less to couple with oxygen, and thus less ATP is produced.
This effect of UCP1 induces shivering and thermogenesis in humans and mice, however there does not seem to be a satisfactory explanation for why dissolution of the H+ gradient causes shivering, simply that it consumes ATP. Thus, the double deficit in ATP could lead to less accumulation of energy in the form of lipid biogenesis, and could also promote increased turnover of food substrates into NADH to make up for the lack of ATP produced.
What I can tell you though, is UCP1 is regulated by two major gene regulators, one called the PPARs, and the other PGC-1a. Both of them increase mitochondria biogenesis and UCP1 expression when upregulated, and they can be upregulated by increased consumption of nitrates, present, as are all healthy things, in leafy vegetables (Inorganic nitrate promotes the browning of white adipose tissue through the nitrate-nitrite-nitric oxide pathway.
). Apart from nitrates, short-term fasting plays quite a role in fat accumulation. I will shortly be publishing on it so I hesitate to say more, but the data is intriguing indeed! The bottom line is that fasting isn’t all bad at all.
So those are environmental factors that affect fat accumulation. I wonder if regulation of all these factors differ by ethnicity as well (not so much in through their diet, but endogenously), and if they correlate to obesity rates across different countries. It would certainly be cool to perform population studies with these parameters but it would be a large undertaking, and such an observation would pale in significance to, say, a world-wide population study on Alzheimers.
There are another few layers of regulation between and after these pathways, and I am currently in the process of determining if and how nitrates can alleviate dysfunction with fat tissue. If this piqued your interest, do follow my research!