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Pathways to Fat

July 1, 2005 02:55 PM

It looks like two different pathways are linked through a cholesterol sensing protein and the linkage makes clear that the body's ability to store fat depends on cross talk between the pathways. When the body senses cholesterol in the diet it activates a fat storage program. LXR is the protein that governs the cross talk between these pathways.

I am largely protected from this cross talk between cholesterol and fat storage because: 1. I radically trim fat from meat and eat the cheapest, lowest fat cuts. This reduces the cholesterol. 2. I grill the meat over an open grate and fire so that the fat runs away from the meat. This sheds cholesterol with the fat. 3. I eat game often, which has low cholesterol. 4. I eat sea food often too and it has little cholesterol. 4. I eat relatively small portions of meat and plenty of bulky vegetables. [I have already broken down our 2 year old disposal, wearing it out on melon skins and tough vegetables. I went out today and bought a one horsepower disposal, the most powerful model I could find. For more on the roughage I throw at my poor disposal see my Three Day Food Diary in the Archives.]

I should say that in just the last day or two I have read of several mechanisms that are claimed to promote obesity; LXR, hyperexcitable brain cells that alarm us to awake from sleep, the "thrifty gene" in several incarnations, insulin, cortsol, and leptin. The list goes on with new additions coming at a high rate.

With so many pathways to obesity, you begin to suspect one of two things.

1. Finding one is where the money is. If you are a scientist and you find a path that some pharmacuetical intervention may alter, you are rich.

2. Evolution seems to have designed redundant pathways to fat storage. This is a bit unusual, I think, for redundancy is expensive and evolutionary structures only show redundancy when it really matters.

Why would fat storage be so important in the evolutionary environment? I tried to answer this in my Why We Get Fat article in the Archives.

A final comment. It is curious that so little research is done on the gene expression triggered by energy expenditure and how these pathways govern fat storage. It is pretty much a no-brainer that energy expenditure has declined by about 45% over the past two decades. Caloric intake has held fairly steady until just recently, where it has begun to explode as a result of soft drink and juice consumption and more eating outside the home. Do we need more research on the energy intake/expenditure part of the equation? I think so.

But, then we have the Lazy Overeater Theorem from my paper. Or, to put it more kindly, the evolutionary rule of energy conservation: Don't Waste Energy -- Eat it when you can and don't spend it if you don't have to. Modern life offers the ease and wealth to give expression to this innate human trait.

Here is some of the text focusing on an evolutionary explanation for the linkage between fat storage and cholesterol sensing from Science Daily showing the linkages between the fat storing and cholesterol sensing/burning pathways.

"From the point of view of evolution, an animal capable of linking its ability to sense cholesterol with its ability to store fat may have had a survival advantage. An adult mammal has virtually no need for dietary cholesterol because its body can synthesize enough on its own. But LXRs give an animal the ability to sense the cholesterol component of a high-fat diet and get rid of it, while retaining the fat and storing it for times of deprivation."

Dr. Mangelsdorf the lead author of the article in Cell Metabolism says, "Our work suggests that fat storage is inextricably linked to the body's ability to metabolize cholesterol and that the LXRs have evolved as the sensors that govern the unique cross talk between these two important metabolic pathways."

· Evolutionary Fitness

Comments

Posted by: Flower Online [TypeKey Profile Page] at September 12, 2006 2:42 AM

> ...evolutionary structures only show

> redundancy when it really matters...

Sthephen J. Gould pointed out that organs with two functions might be one of the key devices on which evolution operates. Darwin also felt strongly about this and expanded on this theme in later editions of the Origin of Species. Similarly, one function may be performed by two organs.

See Gould's "Bully for Brontosaurus" for an essay on the origin of flying wings from heat regulating organs. The argument runs like this: 5% of a wing is useless, so natural selection will have nothing to work on. However, even a slight capacity to expand or contract exposed body area has significant benefits in controlling body heat. So, natural selection favours larger heat regulators but only up to a point; as luck would have it, that point is usually when they begin having a significant aerodynamic effect, and now natural selection will favour better air lift. Gould quotes lab research (someone else's) that supports this.

I would think that at first, flying wings weren't meant to fly as much as they were meant to help jumping and running. You could think of legs and wings being redundant systems for moving about. Eating, and storing food reserves, seem to me pretty basic for survival, so wouldn't it be natural for a flexible and scavenging beast like early man to develop more than one way to store fat?

Cheers,
Vincent

Posted by: Vincent at July 7, 2005 11:32 PM

I think Sattar is on to something. I chose a poor title for this post which misdirected expectations as to content. I really is about all this pathways and the hopes of financial gain if they can be manipulated.

One thing is important, or so it seems at this stage of the research, your body doesn't seem to know there is fat to be stored unless it gets this signal from the presence of cholesterol with the fat.

Posted by: Arthur De Vany at July 1, 2005 6:03 PM

Right about the link between research and Big Pharma.

I thought I really was talking about the pathways to fat and certain curiousities in the research. Probably a poor choice of titles, because I don't worry about cholesterol much either.

One of the articles I mentioned even makes clear that the body triggers a burning response to a cholesterol signal. So, it sheds it quickly and it likely can do no harm.

Posted by: Arthur De Vany at July 1, 2005 5:31 PM

Most studies done on cholesterol in Universities are mainly sponsered by the big Pharmas. Cholesterol may trigger fat accumulation but has not been proven to cause CVD, or link to heart dease directly.

Time to get off the Cholesterol bandwagon, Please.

Posted by: Sattar at July 1, 2005 5:01 PM

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