In a recent study which was published in “Mediators of Inflammation” (1), scientists reported that obesity is associated with a silent yet constantly ongoing inflammation of the body. Generally, we perceive inflammation to be characterized by some form of physical expression such as swelling, itching, the production of heat, pain, redness, or some manifestation which can be seen or felt. But inflammation in our bodies is, in fact, any reactionary response to offensive triggering factor/s; & such inflammation may not even be detectable by our senses! This latter form of inflammation, which best describes the type which besieges an obese individual, is unapparent to us because it occurs at a cellular level (more on that later).
Technically defined as having a BMI of 30 or above, obesity is known to induce the silent inflammation described above & consequently, may have serious & adverse effects on our healths. Obesity-induced inflammation which occurs in fat tissue, has been proven to lead to a host of diseases that plague us today including insulin resistance, type 2 diabetes, heart diseases & immune disorders. Fortunately, some food components have been discovered to have combative abilities against such inflammation. Let's look at the process of inflammation in greater detail, & how food components act to control it.
What causes inflammation in fatty tissue?
Before we delve further, it is important that you understand that these inflammatory responses take place at individual cellular levels within our fatty tissue. To give you a clearer idea - if you think of the spare tire around your belly {BG's comment: oh you know THAT spare tire}, that ream of fatty tissue is made up of hundreds, thousands or even {BG's comment: heaven forbid!} millions of individual fat cells.
The onset of inflammation at the site of an individual fat cell happens as a result of interaction between 2 major players : Macrophages & MCP-1. Macrophages are a type of immune cells within our blood stream & MCP-1 is a substance found to be residing in the individual fat cell. The interaction between these 2 players, & hence inflammation, is described below.
First of all, MCP-1 induces macrophage infiltration from our blood stream into the individual fat cells. Post macrophage infiltration into the fat cell, MCP-1 is also responsible for activating these macrophages to release inflammatory mediators (substances that create inflammation). When released, inflammatory mediators will affect insulin signaling & at the same time, act to increase the production of fatty acids (in particular, harmful saturated fatty acids) within the fat cell. Elevated levels of saturated fatty acids will, in turn, influence our genes to express pro-inflammatory factors that encourage even further inflammatory responses. In this manner, macrophages & MCP-1 interact at the sites of individual fat cells to create a vicious cycle of inflammation within our bodies.
Therefore, it is not surprising to learn that macrophage infiltration is found to be prominent in fat tissue and correlates positively with BMI, fat tissue size as well as total amount of overall body fat in an individual. The presence of MCP-1 is also known to be significantly higher in the obese individual.
How do food components act to control inflammation?
Food components act by targeting various master regulators of inflammatory gene expression, thereby inhibiting the release of various inflammatory mediators.
Master regulators of inflammatory gene expression include firstly, NF-kB & JNK, both of which are important transcription factors i.e. proteins involved in the flow of genetic information; and secondly, PPARy, which is a protein that acts as a receptor for other molecules to bind on to. Food components control mediators of inflammation either by acting to directly influence NF-kB & JNK (PPARy-independent) or indirectly via PPARy (PPARy-dependent).
Therefore, in a PPARy-independent situation, food components act on NF-kB & JNK to suppress mediators of inflammation by direct interference of the flow of genetic information, which in turn results in interruption of the genetic signaling pathways necessary for the inflammatory gene expression.
On the other hand, in a PPARy-dependent scenario, food components work hand in hand with PPARy to exert an anti inflammatory effect. PPARy acts as the lock in a "Lock and Key system" which certain food components can latch onto. This locking action then sets off a chain of molecular mechanisms in the cell, which interferes with the signaling pathways of inflammatory gene expression resulting in suppressed production of inflammatory mediators.
Phew! Now that the hard part is over, here is the good news! So which food components regulate inflammation? As explained, food components can work either dependent or independent of PPARy.
PPARy-dependent food components:
Compound | Origin | Actions |
Abietic Acid | Pine - in rosin fraction of species such as grand fir, lodgepole pine. | Suppress proinflammatory mediators; increase adiponection (hormone which regulates fat metabolism); act with PPARy to mitigate inflammation. |
Auraptene | Citrus Fruits - mainly in peel. | regulate flow of information in genes targeted by PPARy; increase adiponectin secretion; decrease proinflammatory mediators; promote glucose uptake. |
Capsaicin | Hot Pepper | induce thermogenisis & fat oxidation; decreases secretion of inflammatory mediators, increases expression of adiponectin; suppresses macrophage migration and activation, improves insulin resistance. |
Dehydroabietic Acid | Pine Rosin | PPARy agonist - binds to & acts like PPARy. |
Isohumulone | Hummulus Lupulus | PPARy agonist. |
Isoprenoid | Herbs | anti-tumor proliferation, anti-diabetes, controls cholesterol. |
Resveratrol | Red Wine (dont u love this) | PPARy agonist. |
6-Shogaol | Ginger | Acts with PPARy to increase production of adiponectin. |
PPARy-independent food components:
Compound | Origin | Actions |
Anthocyanin | Red/Purplish Fruit such as grapes, blueberries; apples; beans. | Anti-oxidant; inhibition of inflammatory mediators. |
Diosgenin | Fenugreek; wild yam. | Suppress inflammatory mediators induced by interaction between fat cells & macrophages. |
6-Gingerol | Ginger | increase adiponectin, a hormone which regulates fat metabolism. |
Luteolin | Medicinal plants; some vegetables & fruits. | Anti-oxidant; anti-inflammatory; anti-allergy; inhibit JNK activity in macrophages. |
Naringenin | Citrus fruits | Inhibit inflammation caused by interaction between fat cells & macrophages. |
Naringenin Chalcone | Tomato peel | same effect as Naringenin, only more significant. |
Polyunsaturated Fatty Acids | Fish Oil | Anti-obesity; anti-inflammatory factors. However, requires cofactors such as folic acid, vitamins, minerals, L-arginine (a protein) for anti-inflammatory actions. |
Conclusion:
By learning how compounds derived from food sources regulate inflammation in fat cells, we may have seeded various new & natural avenues to managing inflammatory related diseases caused by obesity, such as diabetes & cardiovascular diseases.
In the same vein, another recent study published in the Journal of Obesity, "Anti-Inflammatory Nutrition as a Pharmalogical Approach to treat Obesity" (2), the researchers have also concluded that a food based anti-inflammatory approach, which targets & suppresses inflammation in our bodies, could be used in conjunction with conventional drugs to enhance the treatment of obesity.
In view of the rising socio-economic costs of waging an uphill fight against epidemic obesity & related diseases, these studies bring renewed hopes for a more holistic, cheaper & hopefully, more effective solution for containing the spiraling situation
Sources:
(1)Shizuka Hirai, Nobuyuki Takahashi, Tsuyoshi Goto, Shan Lin, Taku Uemura, Rina Yu, Teruo Kawada (March, 2010). Functional Food Targeting the Regulation of Obesity-Induced Inflammatory Responses and Pathologies. Mediators of Inflammation. Hidawi Publishing Corporation. Vol 2010; Article 367838.
(2) Barry Sears, Camillo Ricordi (May, 2010). Anti-Inflammatory Nutrition as a Pharmalogical Approach to Treat Obesity. Journal 0f Obesity. Hidawi Publishing Corporation. Vol 2011; Article 431985.
No comments:
Post a Comment