| ||||||||||||||
 |
||||||||||||||
|
Home > University > Biology > The role of different adipose tissue depots in insulin resistance The role of different adipose tissue depots in insulin resistanceYou can download this essay for free. All you need to do is register and submit at least one of your essays to us. Or you can purchase this essay for just $2 instantly without registering
Downloads to date:
N/A
| Words: 5512 | Submitted: 27-Dec-2011 This is what the first 3 pages of the essay look like    DescriptionThe adipose tissue is unevenly distributed in the body in both lean and obese individuals, giving rise to distinct biochemical properties of different fat compartments. Which depots fat preferentially accumulates in is influenced by a number of factors such as age, gender, ethnicity, genetics, lifestyle, degree of obesity and hormonal profile. Precise mechanisms of a relationship between fat deposition and insulin resistance are still being elucidated, but a significant link has been made between upper body obesity and adversary health outcomes such as diabetes.PreviewThe role of different adipose tissue depots in insulin resistanceContents Page Abbreviations ...............................................................................................................3 Introduction ...................................................................................................................4 Adipose tissue metabolism ...........................................................................................5 Insulin resistance ...........................................................................................................6 Adipose tissue partitioning .............................................................................................7 Factors influencing lipid partitioning pattern ...................................................................7 Depot locations ...............................................................................................................8 Complications associated with fat excess in specific depots ..........................................9 Obesity-enhanced insulin resistance ..............................................................................11 Inflammation ...................................................................................................................13 VAT and SAT depot profiles ...........................................................................................14 Molecular mechanisms important in obesity-induced insulin resistance ........................16 Other molecules associated with abnormalities of different fat depots............................19 Conclusion .......................................................................................................................21 Abbreviations AR Adrenoreceptors CVD Cardiovascular disease DSAT Deep subcutaneous adipose tissue FFA Free fatty acids HSL Hormone-senstive lipase IL Interleukin IRS Insulin receptor substrates MCP1 Monocyte chemotactic protein MS Metabolic Syndrome PPAR Peroxisome proliferator-activated receptor SAT Subcutaneous adipose tissue SSAT Superficial subcutaneous adipose tissue TG Triglycerides TLR Toll-like receptors TNF ? Tumour necrosis factor ? VAT Visceral adipose tissue VLDL Very low density lipoprotein UPR Unfolded protein response Introduction The adipose tissue is unevenly distributed in the body in both lean and obese individuals, giving rise to distinct biochemical properties of different fat compartments. Which depots fat preferentially accumulates in is influenced by a number of factors such as age, gender, ethnicity, genetics, lifestyle, degree of obesity and hormonal profile. Precise mechanisms of a relationship between fat deposition and insulin resistance are still being elucidated, but a significant link has been made between upper body obesity and adversary health outcomes such as diabetes. Evolutionary, accumulation of fat is advantageous for surviving periods of food shortage, as the Thrifty Gene Hypothesis suggests, but with the rise in availability of food and a lack of physical activity, storage of fat becomes excessive and leads to greater incidence of obesity (1). There is a 9% increase in obesity in England since 1993 (2). Incidence of diabetes is predicted to increase by 4.4% globally, mostly due to a positive correlation between weight gain and insulin resistance (3). For every kilogram of weight gain, risk of diabetes increases 4-9% . Obese individuals (BMI > 30 kg/m2) are susceptible to a variety of metabolic abnormalities, collectively known as the Metabolic Syndrome (MS). These include hyperglycemia, dyslipidemia, hyperinsulinemia, hypertension, which enhance the danger of cardiovascular disease (CVD) and Diabetes Mellitus. (4) When people survive off high-fat diets, there is an excess in fatty acid supply and a reduction in lipid oxidation, which increases adipose tissue mass by increasing size and number of adipocytes. (5) Excess calories are preferentially stored in subcutaneous adipose tissue (SAT) but when they can no longer recruit preadipocytes and store lipids, fat spills-over into other depots, mainly visceral adipose tissue (VAT) depot and into other insulin-sensitive tissues (e.g. liver). It is this kind of lipid partitioning that determines whether obese individuals develop insulin resistance and glucose intolerance with visceral obesity is a major risk factor for developing insulin resistance associated problems (6). Adipose tissue metabolism Adipose tissue is vital for storage of energy in the form of triglycerides (TG) for periods when fuel is not readily available, e.g. during exercise. It is now also viewed as a dynamic endocrine tissue ... Download this essay in full now!Just upload at one of your essays to our database and instantly download your selection! Registration takes secondsOr you can download this essay for $2 immediately without registeringComments and reviewsReviews are written by members who have downloaded the essay No comments yet. If you download the essay you can review it afterwards. |
|||||||||||||
