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== Causes ==
== Causes ==
The immediate cause of obesity is net energy imbalance — the organism consumes more usable calories than it expends, wastes, or discards via elimination. The fundamental cause of obesity is not well understood, but is presumably a combination of the organism's [[genetics|genes]] and [[Environment (biophysical)|environment]]. There is a growing consensus that, in humans, central obesity is related to the excessive consumption of fructose.<ref>{{cite journal|last=Elliott|first=Sharon|coauthors=Nancy L Keim, Judith S Stern, Karen Teff and Peter J Havel|title=Fructose, weight gain, and the insulin resistance syndrome|journal=American Journal of Clinical Nutrition|date=2002|year=2002|month=November|volume=76|issue=5|pages=911-922|url=http://www.ajcn.org/content/76/5/911.full}}</ref> <ref>{{cite journal|last=Perez-Pozo|first=SE|coauthors=et al|title=Excessive fructose intake induces the features of metabolic syndrome in healthy adult men: role of uric acid in the hypertensive response|journal=International Journal of Obesity|date=22|year=2009|month=December|volume=34|pages=454-461|doi=10.1038|url=http://www.gnmhealthcare.com/pdf/12-2009/22/ijo_vaop_ncurrent_gnm_ijo2009259a.pdf}}</ref><ref>{{cite journal|last=Choi|first=Mary|title=The Not-so-Sweet Side of Fructose|journal=JASN|year=2009|month=March|volume=20|series=3|pages=457-459|doi=10.1681|url=http://jasn.asnjournals.org/content/20/3/457.full}}</ref> Other environmental factors, such as maternal smoking, estrogenic compounds in the diet and endocrine disrupting chemicals may be important also.<ref>{{cite journal|last=Heindel|first=Jerrold|title=The Obesogen Hypothesis of Obesity: Overview and Human Evidence|journal=Endocrine updates|year=2011|volume=30|series=4|pages=355-365|doi=10.1007/978-1-4419-7034-3_17|url=http://www.springerlink.com/content/q5487k0r18162473/}}</ref>
The immediate cause of obesity is net energy imbalance — the organism consumes more usable calories than it expends, wastes, or discards via elimination. The fundamental cause of obesity is not well understood, but is presumably a combination of the organism's [[genetics|genes]] and [[Environment (biophysical)|environment]].


Hypercortisolism, such as in [[Cushing's syndrome]] also leads to central obesity. Many prescription drugs can also have side effects resulting in obesity{{Citation needed|date=December 2009}}.
Hypercortisolism, such as in [[Cushing's syndrome]] also leads to central obesity. Many prescription drugs, such as dexamethasone and other steroids, can also have side effects resulting in [[central obesity]]<ref>{{cite journal|last=Bujalska|first=Iwona|coauthors=et al|title=Does central obesity reflect “Cushing's disease of the omentum”?|journal=The Lancet|date=26|year=1997|month=April|volume=Volume 349|issue=9060,|pages=1210-1213|doi=10.1016/S0140-6736(96)11222-8}}</ref>, especially in the presence of elevated insulin levels.


Because fat in the midsection contains the greatest amount of cortisol receptors, fat is created and stored in the midsection, specifically in fat cell deposits deep in the abdomen.<ref>[http://www.natural-weight-loss-myths-revealed.com/cortisol-and-weight-gain.html Cortisol and Belly Fat]</ref>
Because fat in the midsection contains the greatest amount of cortisol receptors, fat is created and stored in the midsection, specifically in fat cell deposits deep in the abdomen.<ref>[http://www.natural-weight-loss-myths-revealed.com/cortisol-and-weight-gain.html Cortisol and Belly Fat]</ref>

Revision as of 06:03, 1 August 2011

Abdominal obesity
SpecialtyEndocrinology Edit this on Wikidata

Abdominal obesity, colloquially known as belly fat or clinically as central obesity, is the accumulation of abdominal fat resulting in an increase in waist size. There is a strong correlation between central obesity and cardiovascular disease.[1]

Visceral fat, also known as organ fat or intra-abdominal fat, is located inside the peritoneal cavity, packed in between internal organs and torso, as opposed to subcutaneous fat which is found underneath the skin, and intramuscular fat which is found interspersed in skeletal muscle. Visceral fat is composed of several adipose depots including mesenteric, epididymal white adipose tissue (EWAT) and perirenal fat. An excess of visceral fat is known as central obesity, the "pot belly" or "beer belly" effect, in which the abdomen protrudes excessively. This body type is also known as "apple shaped", as opposed to "pear shaped", in which fat is deposited on the hips and buttocks.

Causes

The immediate cause of obesity is net energy imbalance — the organism consumes more usable calories than it expends, wastes, or discards via elimination. The fundamental cause of obesity is not well understood, but is presumably a combination of the organism's genes and environment. There is a growing consensus that, in humans, central obesity is related to the excessive consumption of fructose.[2] [3][4] Other environmental factors, such as maternal smoking, estrogenic compounds in the diet and endocrine disrupting chemicals may be important also.[5]

Hypercortisolism, such as in Cushing's syndrome also leads to central obesity. Many prescription drugs, such as dexamethasone and other steroids, can also have side effects resulting in central obesity[6], especially in the presence of elevated insulin levels.

Because fat in the midsection contains the greatest amount of cortisol receptors, fat is created and stored in the midsection, specifically in fat cell deposits deep in the abdomen.[7]

Diagnosis

While central obesity can be obvious just by looking at the naked body (see the picture), the severity of central obesity is determined by taking waist and hip measurements. The absolute waist circumference (>102 centimetres (40 in) in men and >88 centimetres (35 in) in women) and the waist-hip ratio (>0.9 for men and >0.85 for women)[8] are both used as measures of central obesity. A differential diagnosis includes distinguishing central obesity from ascites and intestinal bloating. In the cohort of 15,000 people participating in the National Health and Nutrition Examination Survey (NHANES III), waist circumference explained obesity-related health risk better than the body mass index (or BMI) when metabolic syndrome was taken as an outcome measure and this difference was statistically significant. In other words, excessive waist circumference appears to be more of a risk factor for metabolic syndrome than BMI.[9] Another measure of central obesity which has shown superiority to BMI in predicting cardiovascular disease risk is the Index of Central Obesity (waist-to-height ratio - WHtR), where a ratio of >=0.5 (i.e. a waist circumference at least half of the individual's height) is predictive of increased risk.[10]

An increasing acceptance of the importance of central obesity within the medical profession as an indicator of health risk has led to new developments in obesity diagnosis such as the Body Volume Index, which measures central obesity by measuring a person’s body shape and their weight distribution.

Index of Central Obesity

Index of Central Obesity (ICO) is the ratio of waist circumference and height first proposed by a Parikh et al in 2007[11][12] as a better substitute to the widely-used waist circumference in defining metabolic syndrome.[13] The National Cholesterol Education Program Adult Treatment Panel III suggested cut off of 102 cm and 88 cm for males and females as a marker of central obesity.[14] The same was used in defining metabolic syndrome.[15] Misra et al. suggested that these cutoffs are not applicable among Indians and the cutoffs be lowered to 90 cm and 80 cm for males and females.[16] Various race specific cutoffs were suggested by different groups.[citation needed] The International Diabetes Federation defined central obesity based on these various race and gender specific cutoffs.[citation needed] The other limitation of waist circumference is that it can not be applied in children.[dubious – discuss]

Parikh et al looked at the average heights of various races and suggested that by using ICO various race- and gender-specific cutoffs of waist circumference can be discarded.[13] An ICO cutoff of more than 0.5 is suggested as a criteria to define central obesity.[citation needed] Parikh et al further tested a modified definition of of metabolic syndrome in which waist circumference was replaced with ICO in the National Health and Nutrition Examination Survey (NHANES) database and found the modified definition to be more specific and sensitive.[13]

This parameter has been used in the study of metabolic syndrome[17][18] and cardiovascular disease.[19]

Body Volume Index

BVI is based upon the principle that excess abdominal weight, measured by part volume as a percentage of total volume, constitutes a greater health risk. Recent validation has concluded that total and regional body volume estimates correlate positively and significantly with biomarkers of cardio-vascular risk and BVI calculations correlate significantly with all biomarkers of cardio-vascular risk.[20]

Health risks

Excess adipose tissue on a male

Central obesity is associated with a statistically higher risk of heart disease, hypertension, insulin resistance, and Diabetes Mellitus Type 2 (see below). Belly fat is a symptom of metabolic syndrome, and is an indicator used in the diagnosis of that disorder.[21][22][23]

Central obesity can be a feature of lipodystrophies, a group of diseases which is either inherited, or due to secondary causes (often protease inhibitors, a group of medications against AIDS). Central obesity is a symptom of Cushing's syndrome[24] and is also common in patients with polycystic ovary syndrome (PCOS). Central obesity is associated with glucose intolerance and dyslipidemia.

Relationship with diabetes

There are numerous theories as to the exact cause and mechanism in Type 2 Diabetes. Central obesity is known to predispose individuals for insulin resistance. Abdominal fat is especially active hormonally, secreting a group of hormones called adipokines that may possibly impair glucose tolerance.

Insulin resistance is a major feature of Diabetes Mellitus Type 2 (T2DM), and central obesity is correlated with both insulin resistance and T2DM itself.[25][26] Increased adiposity (obesity) raises serum resistin levels,[27][28][29][30] which in turn directly correlate to insulin resistance.[31][32][33][34] Studies have also confirmed a direct correlation between resistin levels and T2DM.[27][35][36][37] And it is waistline adipose tissue (central obesity) which seems to be the foremost type of fat deposits contributing to rising levels of serum resistin.[38][39] Conversely, serum resistin levels have been found to decline with decreased adiposity following medical treatment.[40]

Relationship with Alzheimer's Disease

A US study reported in May 2010 Annals of Neurology examining over 700 adults found evidence to suggest higher volumes of visceral fat, regardless of overall weight, were associated with smaller brain volumes and increased risk of dementia.[41][42][43]

Measurement

Silhouettes and waist circumferences representing normal, overweight, and obese

There are various ways of measuring abdominal obesity including:

In those with a BMI under 35, intra-abdominal body fat is related to negative health outcomes independent of total body fat.[45] Intra-abdominal or visceral fat has a particularly strong correlation with cardiovascular disease.[8]

Sex differences

Female sex hormone causes fat to be stored in the buttocks, thighs, and hips in women. Men are more likely to have fat stored in the belly due to sex hormone differences. When women reach menopause and the estrogen produced by ovaries declines, fat migrates from their buttocks, hips and thighs to their waists;[46] later fat is stored in the belly.[47]

Prevention and treatments

Performing adequate aerobic exercise and eating a healthy diet can prevent central obesity, and losing weight via these methods is the main way to reverse the condition.[48][unreliable source?]

Adjunctive therapies which may be prescribed by a physician are orlistat or sibutramine, although the latter has been associated with increased cardiovascular events and strokes and has been withdrawn from the market in the United States,[49] the UK,[50] the EU,[51] Australia,[52] Canada,[53] Hong Kong,[54] Thailand[55] and Mexico.

In the presence of diabetes mellitus type 2, the physician might instead prescribe metformin and thiazolidinediones (rosiglitazone or pioglitazone) as anti-diabetic drugs rather than sulfonylurea derivatives. Thiazolidinediones may cause slight weight gain but decrease "pathologic" abdominal fat, and therefore may be prescribed for diabetics with central obesity.[56]

Sit-ups myth

There is a common misconception that spot exercise (that is, exercising a specific muscle or location of the body) most effectively burns fat at the desired location, but this is not the case. Spot exercise is beneficial for building specific muscles, but it has little effect, if any, on fat in that area of the body, or on the body's distribution of body fat. The same logic applies to sit-ups and belly fat. Sit-ups, crunches and other abdominal exercises are useful in building the abdominal muscles, but they have little effect, if any, on the adipose tissue located there.[57]

Slang terms

File:Love-Handles.jpg
Excess abdominal fat on a male.

Several colloquial terms used to refer to central obesity, and to people who have it, refer to beer drinking. However, there is little scientific evidence that beer drinkers are more prone to abdominal obesity, despite it being known colloquially as "beer belly", "beer gut", or "beer pot". One of the few studies conducted on the subject did not find that beer drinkers are more prone to abdominal obesity than nondrinkers or drinkers of wine or spirits.[58][59] Chronic alcoholism can lead to cirrhosis, symptoms of which include gynecomastia (enlarged breasts) and ascites (abdominal fluid). These symptoms can suggest the appearance of central obesity.

"Love handles" and "spare tyre" (or "spare tire") are colloquial terms for deposits of fat around a person's midsection, especially visible on the sides over the abdominal external oblique muscle. Love handles are visible deposits on each side of the abdomen or lower back (that a hypothetical lover might grab to pull the subject into an embrace); a spare tire appears to encircle the abdomen (thus resembling an automobile tire).

"Muffin top" is a pejorative term used for a person whose midsection spills over the waistline of his or her trousers in a manner that resembles the top of a muffin spilling over its baking pan.

"Pot belly" is another colloquial term used to describe a person who has an excessive amount of abdominal fat. This is especially pronounced and visible over clothing and may be indicative of other health related problems.

See also

Further reading

  • Griesemer, Rebecca Lynn (July 25, 2008). Index of Central Obesity as a Parameter to Evaluate Metabolic Syndrome for White, Black, and Hispanic Adults in the United States (Master's thesis). Georgia State University.
  • Lee, Kayoung; Song, Yun-Mi; Sung, Joohon (2008). "Which Obesity Indicators Are Better Predictors of Metabolic Risk?: Healthy Twin Study". Obesity. 16 (4): 834–40. doi:10.1038/oby.2007.109. PMID 18239595.
  • Shao, J.; Yu, L.; Shen, X.; Li, D.; Wang, K. (2010). "Waist-to-height ratio, an optimal predictor for obesity and metabolic syndrome in Chinese adults". The Journal of Nutrition, Health & Aging. 14 (9): 782–5. doi:10.1007/s12603-010-0106-x. PMID 21085910.

References

  1. ^ Yusuf S, Hawken S, Ounpuu S, Dans T, Avezum A, Lanas F, McQueen M, Budaj A, Pais P, Varigos J, Lisheng L, INTERHEART Study Investigators. (2004). "Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (the INTERHEART study): case-control study". Lancet. 364 (9438): 937–52. doi:10.1016/S0140-6736(04)17018-9. PMID 15364185.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  2. ^ Elliott, Sharon (2002). "Fructose, weight gain, and the insulin resistance syndrome". American Journal of Clinical Nutrition. 76 (5): 911–922. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |month= ignored (help)CS1 maint: date and year (link)
  3. ^ Perez-Pozo, SE (22). "Excessive fructose intake induces the features of metabolic syndrome in healthy adult men: role of uric acid in the hypertensive response" (PDF). International Journal of Obesity. 34: 454–461. doi:10.1038. {{cite journal}}: Check |doi= value (help); Check date values in: |date= and |year= / |date= mismatch (help); Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |month= ignored (help)
  4. ^ Choi, Mary (2009). "The Not-so-Sweet Side of Fructose". JASN. 3. 20: 457–459. doi:10.1681. {{cite journal}}: Check |doi= value (help); Unknown parameter |month= ignored (help)
  5. ^ Heindel, Jerrold (2011). "The Obesogen Hypothesis of Obesity: Overview and Human Evidence". Endocrine updates. 4. 30: 355–365. doi:10.1007/978-1-4419-7034-3_17.
  6. ^ Bujalska, Iwona (26). "Does central obesity reflect "Cushing's disease of the omentum"?". The Lancet. Volume 349 (9060, ): 1210–1213. doi:10.1016/S0140-6736(96)11222-8. {{cite journal}}: |volume= has extra text (help); Check date values in: |date= and |year= / |date= mismatch (help); Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |month= ignored (help)CS1 maint: extra punctuation (link)
  7. ^ Cortisol and Belly Fat
  8. ^ a b c Yusuf S, Hawken S, Ounpuu S, Dans T, Avezum A, Lanas F, McQueen M, Budaj A, Pais P, Varigos J, Lisheng L, INTERHEART Study Investigators. (2004). "Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (the INTERHEART study): Case-control study". Lancet. 364 (9438): 937–52. doi:10.1016/S0140-6736(04)17018-9. PMID 15364185.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  9. ^ Smith, Sidney C.; Haslam, David (2007). "Abdominal obesity, waist circumference and cardio­metabolic risk: awareness among primary care physicians, the general population and patients at risk – the Shape of the Nations survey". Current Medical Research and Opinion. 23: 379–84. doi:10.1185/030079906X159489. {{cite journal}}: soft hyphen character in |title= at position 50 (help)
  10. ^ Knowles, K. M.; Paiva, L. L.; Sanchez, S. E.; Revilla, L.; Lopez, T.; Yasuda, M. B.; Yanez, N. D.; Gelaye, B.; Williams, M. A. (2011). "Waist Circumference, Body Mass Index, and Other Measures of Adiposity in Predicting Cardiovascular Disease Risk Factors among Peruvian Adults". International Journal of Hypertension. 2011: 1–10. doi:10.4061/2011/931402.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  11. ^ a b Parikh, Rakesh M; Menon, Padmavathy S; Shah, Nalini S; Shah, N (2007). "Index of central obesity – A novel parameter". Medical Hypotheses. 68 (6): 1272–5. doi:10.1016/j.mehy.2006.10.038. PMID 17156939.
  12. ^ Méthot, Julie; Houle, Julie; Poirier, Paul (2010). "Obesity: how to define central adiposity?". Expert Review of Cardiovascular Therapy. 8 (5): 639–44. doi:10.1586/erc.10.38. PMID 20450297.
  13. ^ a b c Parikh, Rakesh M.; Joshi, Shashank R.; Pandia, Kirti (2009). "Index of Central Obesity Is Better Than Waist Circumference in Defining Metabolic Syndrome". Metabolic Syndrome and Related Disorders. 7 (6): 525–8. doi:10.1089/met.2008.0102. PMID 19558273.
  14. ^ a b National Cholesterol Education Program (2002). Third Report of the Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (ATP III Final Report). National Institutes of Health. p. II–17.
  15. ^ National Cholesterol Education Program (2002). Third Report of the Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (ATP III Final Report). National Institutes of Health. p. II–27.
  16. ^ Misra, Anoop; Wasir, Jasjeet S.; Vikram, Naval K.; Pandey, Ravindra M.; Kumar, Pawan (2010). "Cutoffs of Abdominal Adipose Tissue Compartments as Measured by Magnetic Resonance Imaging for Detection of Cardiovascular Risk Factors in Apparently Healthy Adult Asian Indians in North India". Metabolic Syndrome and Related Disorders. 8 (3): 243–7. doi:10.1089/met.2009.0046. PMID 20156066. {{cite journal}}: Unknown parameter |unused_data= ignored (help)
  17. ^ Joshi, P. P. (2008). "Is Waist to Height Ratio a Better and More Practical Measure of Obesity to Assess Cardiovascular or Diabetes risk in Indians?". Journal of Association of Physicians of India. 56: 202–3, author reply 203–4. PMID 18700281.
  18. ^ Veigas, Nina Maria; Dharmalingam, Mala; Marcus, Sara Rani (2011). "Oxidative Stress in Obesity and Metabolic Syndrome in Asian Indians". Journal of Medical Biochemistry. 30 (2): 115–20. doi:10.2478/v10011-011-0006-6.
  19. ^ Gupta, R; Rastogi, Priyanka; Sarna, M; Gupta, VP; Sharma, SK; Kothari, K (2007). "Body-Mass Index, Waist-Size, Waist-Hip Ratio and Cardiovascular Risk Factors in Urban Subejcts". Journal of Association of Physicians of India. 55: 621–7. PMID 18051732.
  20. ^ Romero-Corral, A. Somers, V. Lopez-Jimenez, F. Korenfeld, Y. Palin, S. Boelaert, K. Boarin, S. Sierra-Johnson, J. Rahim, A. (2008) 3-D Body Scanner, Body Volume Index: A Novel, Reproducible and Automated Anthropometric Tool Associated with Cardiometabolic Biomarkers Obesity A Research Journal 16 (1) 266-P
  21. ^ Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (2001). "Executive Summary of The Third Report of The National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, And Treatment of High Blood Cholesterol In Adults (Adult Treatment Panel III)". JAMA : the journal of the American Medical Association. 285 (19): 2486–97. doi:10.1001/jama.285.19.2486. PMID 11368702.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  22. ^ Grundy SM, Brewer HB, Cleeman JI, Smith SC, Lenfant D, for the Conference Participants. Definition of metabolic syndrome: report of the National, Heart, Lung, and Blood Institute/American Heart Association conference on scientific issues related to definition. Circulation. 2004;109:433-438.
  23. ^ American Heart Association's description of Syndrome X
  24. ^ Bujalska IJ, Kumar S, Stewart PM (1997). "Does central obesity reflect "Cushing's disease of the omentum"?". Lancet. 349 (9060): 1210–3. doi:10.1016/S0140-6736(96)11222-8. PMID 9130942.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  25. ^ Duman BS, Turkoglu C, Gunay D, Cagatay P, Demiroglu C, Buyukdevrim AS. The interrelationship between insulin secretion and action in type 2 diabetes mellitus with different degrees of obesity: evidence supporting central obesity. Diabetes Butr Metab. 16(4): 243-250, 2003.
  26. ^ Gabriely, I., Ma, X. H., Yang, X. M., Atzmon G, Rajala MW, berg AH, Sherer P, Rossetti L, Barzilai N. Removal of visceral fat prevents insulin resistance and glucose intolerance of aging: an adipokine-mediated process? Diabetes. 51: 2951–2958, 2002.
  27. ^ a b Asensio, C., Cettour-Rose, P., Theander-Carrillo, C., Rohner-Jeanrenaud, F. and Muzzin, P. Changes in glycemia by leptin administration or high-fat feeding in rodent models of obesity/type 2 diabetes suggest a link between resistin expression and control of glucose homeostasis. Endocrinology. 145: 2206–2213, 2004.
  28. ^ Degawa-Yamauchi MBJE, Juliar BE, Watson W, Kerr K, Jones RM, Zhu Q & Considine RV. Serum resistin (FIZZ3) protein is increased in obese humans. Journal of Clinical Endocrinology and Metabolism. 88: 5452–5455, 2003.
  29. ^ Lee, J. H., Bullen, Jr, J. W., Stoyneva, V. L. and Mantzoros, C. S. Circulating resistin in lean, obese and insulin-resistant mouse models: lack of association with insulinemia and glycemia. Am. J. Physiol. Endocrinol. Metab. 288: E625–E632, 2005.
  30. ^ Vendrell J, Broch M, Vilarrasa N, Molina A, Gomez JM, Gutierrez C, Simon I, Soler J & Richart C. Resistin, adiponectin, ghrelin, leptin, and proinflammatory cytokines: relationships in obesity. Obesity Research. 12: 962–971, 2004.
  31. ^ Hirosumi J, Tuncman G, Chang L, Gorgun CZ, Uysal KT, Maeda K, Karin M, Hotamisligil GS. A central role for JNK in obesity and insulin resistance. Nature. 420: 333-336, 2002. [1]
  32. ^ Rajala, M. W., Qi, Y., Patel, H. R., Takahashi N, Banerjee R, Pajvani UB, Sinha MK, Gingerich RL, Scherer PE, Ahima RS. Regulation of resistin expression and circulating levels in obesity, diabetes, and fasting. Diabetes. 53: 1671–1679, 2004.
  33. ^ Silha JV, Krsek M, Skrha JV, Sucharda P, Nyomba BL and Murphy LJ. Plasma resistin, adiponectin and leptin levels in lean and obese subjects: correlations with insulin resistance. Eur. J. Endocrinol. 149: 331-335, 2003.
  34. ^ Smith, S. R., Bai, F., Charbonneau, C., Janderova, L. and Argyropoulos, G. A promoter genotype and oxidative stress potentially link resistin to human insulin resistance. Diabetes 52, 1611–1618, 2003.
  35. ^ Fujinami, A., Obayashi, H., Ohta, K, Ichimura T, Nishimura M, Matsui H, Kawahara Y, Yamazaki M, Ogata M, Hasegawa G, Nakamura N, Yoshikawa T, Nakano K, Ohta M. Enzyme-linked immunosorbent assay for circulating human resistin: resistin concentrations in normal subjects and patients with type 2 diabetes. Clin. Chim. Acta. 339: 57–63, 2004.
  36. ^ McTernan, P. G., Fisher, F. M., Valsamakis, G, Chetty R, Harte A, McTernan CL, Clark PM, Smith SA, Barnett AH, Kumar S. Resistin and type 2 diabetes: regulation of resistin expression by insulin and rosiglitazone and the effects of recombinant resistin on lipid and glucose metabolism in human differentiated adipocytes. J. Clin. Endocrinol. Metab. 88: 6098–6106, 2003.
  37. ^ Steppan CM, Bailey ST, Bhat S, Brown EJ, Banerjee RR, Wright CM, Patel HR, Ahima RS, Lazar MA. The hormone resistin links obesity to diabetes. Nature. 409:307-312, 2001.
  38. ^ McTernan, C. L., McTernan, P. G., Harte, A. L., Levick, P. L., Barnett, A. H. and Kumar, S. Resistin, central obesity, and type 2 diabetes. Lancet. 359: 46–47, 2002.
  39. ^ McTernan, P. G., McTernan, C. L., Chetty, R, Jenner K, Fisher FM, Lauer MN, Crocker J, Barnett AH, Kumar S. Increased resistin gene and protein expression in human abdominal adipose tissue. J. Clin. Endocrinol. Metab. 87: 2407, 2002.
  40. ^ Valsamakis, G., McTernan, P. G., Chetty, R, Al Daghri N, Field A, Hanif W, Barnett AH, Kumar S. Modest weight loss and reduction in waist circumference after medical treatment are associated with favourable changes in serum adipocytokines. Metab. Clin. Exp. 53:430–434, 2004.
  41. ^ "'Beer belly' link to Alzheimer's". BBC News. 2010-05-20.
  42. ^ http://www.msnbc.msn.com/id/23800703/
  43. ^ Stéphanie Debette, MD, PhD, et al "Visceral fat is associated with lower brain volume in healthy middle-aged adults" Annals of Neurology published online 20May2010 [2]
  44. ^ Iribarren, Carlos; Darbinian, Jeanne A.; Lo, Joan C.; Fireman, Bruce H.; Go, Alan S. (2006). "Value of the Sagittal Abdominal Diameter in Coronary Heart Disease Risk Assessment: Cohort Study in a Large, Multiethnic Population". American Journal of Epidemiology. 164 (12): 1150–9. doi:10.1093/aje/kwj341. PMID 17041127.
  45. ^ U.S. Preventive Services Task Force Evidence Syntheses (2000). HSTAT: Guide to Clinical Preventive Services, 3rd Edition: Recommendations and Systematic Evidence Reviews, Guide to Community Preventive Services. ISBN url=http://www.ncbi.nlm.nih.gov/books/bv.fcgi?rid=hstat3.section.36199. {{cite book}}: Check |isbn= value: invalid character (help); Missing pipe in: |isbn= (help)
  46. ^ Researchers think that the lack of estrogen at menopause play a role in driving our fat northward [3]
  47. ^ Abdominal fat and what to do about it
  48. ^ Christian Finn, M.Sc. "The Best Way To Lose Belly Fat". thefactsaboutfitness.com. Retrieved 2010-04-08. There's a growing body of research to show that the fastest way to lose abdominal fat is with a combination of resistance training and aerobic exercise.
  49. ^ Rockoff, Jonathan D.; Dooren, Jennifer Corbett (October 8, 2010). "Abbott Pulls Diet Drug Meridia Off US Shelves". The Wall Street Journal. Retrieved 8 October 2010.
  50. ^ "Top obesity drug sibutramine being suspended". BBC News. 2010-01-22. Retrieved 2010-01-22.
  51. ^ Template:De icon Sibutramin-Vertrieb in der Europäischen Union ausgesetzt [4]. Abbott Laboratories in Germany. Press Release 2010-01-21. Retrieved 2010-01-27
  52. ^ "Sibutramine (brand name Reductil) Information - Australia". Abbott Laboratories. 2010. Retrieved 2010-10-08.
  53. ^ Health Canada Endorsed Important Safety Information on MERIDIA (Sibutramine Hydrochloride Monohydrate): Subject: Voluntary withdrawal of Meridia® (sibutramine) capsules from the Canadian market.
  54. ^ "De-registration of pharmaceutical products containing sibutramine" (Press release). info.gov in Hong Kong. November 2, 2010. Retrieved 2010-11-08.
  55. ^ "Thai FDA reveals voluntary withrawal of sibutramine from the Thai market" (PDF) (Press release). Food and Drug Administration of Thailand. October 20, 2010. Retrieved 2010-12-22.
  56. ^ Fonseca V (2003). "Effect of thiazolidinediones on body weight in patients with diabetes mellitus". Am. J. Med. 115 Suppl 8A (8): 42S–48S. doi:10.1016/j.amjmed.2003.09.005. PMID 14678865.
  57. ^ Michael Jensen, M.D. (2007-01-19). "Belly fat in men: What you need to know". Mayoclinic.com. Retrieved 2008-04-07. Sit-ups will make your abdominal muscles stronger, sure. And, you may look thinner by building your abdominal muscles because you can hold in your belly fat better. But strengthening your stomach muscles alone will not specifically reduce belly fat.
  58. ^ Bobak M, Skodova Z, Marmot M (2003). "Beer and obesity: a cross-sectional study". Eur J Clin Nutr. 57 (10): 1250–3. doi:10.1038/sj.ejcn.1601678. PMID 14506485.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  59. ^ Staff writer (2003-10-12). "Why the beer belly may be a myth". BBC News.
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