How obesity affects cholesterol levels?

[IMYS]

I need to know how obesity affects lipid profile?

And why levels of high-density lipoproteins (HDL) increases and low-density lipoproteins (LDL) decreases?

 

[CharonY]

You got it the wrong way around. Obesity is correlated with decreased HDL and subsequently cardiovascular diseases. The precise mechanisms are still unclear, though.Short answer is that fat tissue and liver metabolism are altered in several pathways which may explain the effects. But overall it is the result of rather complex interactions. A number of key proteins have been identified that may be attributed to the decline in HDL, and it has been speculated that with more fat tissue simply more of these proteins are present. However it has subsequently been shown that there are actually more changes in the tissue of obese people, which makes a straightforward answer quite impossible.

[Phi for All]

It's been a long time since I read up on this, and my knowledge may be outdated. It's my understanding that cholesterol can be manufactured by the cells, as well as being drawn from the blood stream via LDL receptors. If there are no receptors out for cholesterol, the LDL packets can end up collecting on the walls of the vessels. That's where HDL packets come in, retrieving the cholesterol from the LDL packets and bringing it back into circulation.

 

Iirc, one of the hormones that can cause cells to produce their own cholesterol is insulin. In an obese person with high cholesterol, who also has high blood sugar and thus more insulin, might that not result in much of their dietary cholesterol falling to the vessel walls as LDL?

[IMYS]

I need to know how obesity affects lipid profile?

And why levels of high-density lipoproteins (HDL) increases and low-density lipoproteins (LDL) decreases?

 

Sorry, i mean the opposite (HDL descreases and LDL increases)

It's been a long time since I read up on this, and my knowledge may be outdated. It's my understanding that cholesterol can be manufactured by the cells, as well as being drawn from the blood stream via LDL receptors. If there are no receptors out for cholesterol, the LDL packets can end up collecting on the walls of the vessels. That's where HDL packets come in, retrieving the cholesterol from the LDL packets and bringing it back into circulation.

 

Iirc, one of the hormones that can cause cells to produce their own cholesterol is insulin. In an obese person with high cholesterol, who also has high blood sugar and thus more insulin, might that not result in much of their dietary cholesterol falling to the vessel walls as LDL?

 

So, the high levels of LDL cholesterol is because the lower HDL cholesterol levels?

 

Obesity -> low HDL levels -> high LDL levels ?

[Phi for All]

So, the high levels of LDL cholesterol is because the lower HDL cholesterol levels?

 

Obesity -> low HDL levels -> high LDL levels ?

 

Simply said, the lipoproteins that surround cholesterol for blood transport have two basic jobs in this context, bringing cholesterol to the cells (LDL), and rescuing cholesterol that has gone unclaimed and fallen to the vessel walls (HDL). Normally, our cells have their receptors switched on (like putting out the "Welcome!" mat on the doorstep), looking for an LDL packet of cholesterol. They make the exchange and all is good.

 

If the cells are influenced by hormones like insulin, they switch those receptors off and produce their own cholesterol. Then the LDL packets go unclaimed. HDL packets are empty until they find LDL packets on the vessel walls, where they rescue the cholesterol and put it back into the cycle.

 

If an obese person is eating foods with lots of cholesterol, as well as eating food with lots of sugars that trigger insulin production, then much of the cholesterol will go unwanted and become trapped in LDL packets on the vessel walls. Enough HDL packets in the bloodstream would correct this, but obese people are working against their own systems. The ways to increase HDL are to be more active, lose excess weight, stop smoking cigarettes and drinking alcohol, and eat healthier foods all around.

 

So yes, it all works against the obese person because high LDL levels overwhelm low HDL levels and prevent the system from fixing itself in the normal way. HDL might never be needed to save the day if the cells would stop pulling in the "Welcome!" mat and start participating in the exchange with LDLs more cooperatively.

 

Please note this is perhaps oversimplified, and there is better clinical terminology, but I wanted to explain it in a way that dispels the "good cholesterol vs bad cholesterol" misunderstanding. LDL isn't bad normally, it's the way you should be getting this essential substance. I do hope this information is still accurate, and that one of our experts will correct me if it isn't.

[Psilociraptor]

Contrary to popular belief there is actually a lot of doubt that dietary cholesterol has any direct affect on serum levels. There is no real consensus on the pathogenesis of metabolic syndrome but Patrice D Cani sheds some interesting and revolutionary insight http://diabetes.diabetesjournals.org/content/56/7/1761 From this and other papers the best understanding I could gather is that contrary to maintream dogma, metabolic syndrome is not a nutritional disorder directly but an acute phase response mechanism to infection. In regards to diet, high-fat diets selectively feed inflammatory gut-microbiota leading to over growth, disregulation of intestinal tight junction proteins, and the absorption of endotoxins (immunostimulatory bacterial cell-wall components) across the cell wall. This stimulates a systemic inflammatory response analogous to a low grade sepsis. As with true sepsis dramatic metabolic changes occur to attempt to fight the infection. Leptin is secreted which inhibits hunger. It is believed that this is an attempt to starve off the pathogen (hence why you often have no appetite when you run a fever). However, during the chronic phases leptin resistance occurs to counteract starvation. Leptin resistance is then a likely contributor for eating disorders and obesity. Insulin resistance, cholesterol synthesis and VLDL synthesis are also upregulated during endotoxin challenge. Insulin resistance likely serves as a mechanism to preserve glucose during stress response for reductive biosynthesis and redox maintenance. This allows the body to heal damaged tissues, proliferate immune cells, secrete peroxides against infection, and maintain glutathione function against oxidative stress. The roles of cholesterol and VLDL are less understood. However, it is known that lipoproteins associate with endotoxin binding proteins and therefor serve a dual purpose of distributing lipids and detoxifying lipophilic endotoxins. Hence why lipoproteins embed in the vascular tissue due to its susceptibility to damage by inflammation and infectious microorganisms. Why HDL decreases and LDL increases is not exactly known. Lipoprotein remodeling and HDL/LDL association have been shown to transfer endotoxins in vitro. So there is the possibility that these alterations in lipoprotein profile reflect functional behaviors aimed at channeling immunogenic materials back to the liver.

 

So in short it's not so much that obesity causes lipoprotein alterations. There is the fact that adipose tissue excretes inflammatory signals and there may be a secondary affect on metabolism as a result, but both obesity and lipoprotein alterations occur as downstream effects of inflammatory cascades.