Research articles
 

By Dr. Adel A Al-johari.
Corresponding Author Dr. Adel A Al-johari.
Consultant General and Laparoscopic Surgeon. King abdul Azez University.Jeddah .K S A., P O BOX80215. Jeddah 21589. K S A. - Saudi Arabia 00
Submitting Author Dr. Christine N Grace
GENERAL MEDICINE

Obesity, Diabetes Mellitus, Metabolic Diseases, Insulin Resistance, Fatty Liver

Al-johari. AA. Prospective Incidence Study of Diabetes Mellitus in Morbidly Obese Saudi Patients. WebmedCentral GENERAL MEDICINE 2011;2(5):WMC001927
doi: 10.9754/journal.wmc.2011.001927
No
Submitted on: 16 May 2011 08:13:42 AM GMT
Published on: 18 May 2011 10:20:44 AM GMT

Abstract


Objective: The aim of this study is to evaluate the association between obesity and diabetes mellitus in a sample of morbidly obese Saudi patients.
Design: 201 morbidly obese patients undergoing surgery for obesity were preoperatively assessed. Assessment included complete blood picture, liver enzymes, lipid profile, blood sugar and hormones. Blood pressure was measured and liver ultrasound was done.
Results: 198 patients were enrolled in the study, from which 46 persons (23.23%) were diabetics and 22 (11.11%) were hypertensive. The body mass index (BMI) of both diabetic and non diabetic groups was of significance (p-value = 0.108). Obesity has proven to appear more in childhood 141 (71.21%), followed by in adults 30 (15.15%) and then at the age of puberty 17 ( 8.58%). There was a high significance (p-value = 0.005) in morbidly obese hypertensive patients having diabetes than in morbidly obese patients with normal blood pressure and do not suffer from diabetes.
Conclusion: Obesity is becoming a major health problem as it is considered a risk factor in metabolic diseases. It is also becoming more popular in children increasing the incidence of its morbidity disorders due to the longer exposure. Abdominal obesity is a recognized risk factor for both type 2 diabetes mellitus and cardiovascular disease resulted in the metabolic consequences of obesity, such as insulin resistance and impaired glucose tolerance. In summary, fatty liver is relatively common in overweight and obese volunteers with type 2 diabetes mellitus (DM) and is an aspect of body composition related to severity of insulin resistance, dyslipidemia, and inflammatory markers.

Introduction


Obesity is a medical condition in which excess body fat has accumulated to the extent that it may have an adverse effect on health, leading to reduced life expectancy and/or increased health problems.[i]
Body mass index (BMI), a measurement which compares weight and height, defines people as overweight (pre-obese) when their BMI is between 25 kg/m2 and 30 kg/m2, and obese when it is greater than 30 kg/m2.[ii]
Obesity is most commonly caused by a combination of excessive dietary calories, lack of physical activity, and genetic susceptibility, although a few cases are caused solely by genes, endocrine disorders, medications or psychiatric illness.[iii] [iv]
Obesity has reached epidemic proportions globally, with more than 1 billion adults overweight - at least 300 million of them clinically obese. The health implications posed by this condition involve a wide spectrum of disease states, including diabetes, steatohepatitis/nonalcoholic fatty liver disease (NAFLD), cholelithiasis, and hypertension, as well as neuromuscular and cardiovascular complications.[v] 
A significant association between DM and obesity has been noted in several epidemiological studies. Considerable evidence has suggested that excessive weight gain is the most common cause DM. This association has been observed in several populations, in different regions of the world. Obesity-hypertension, a term that underscores the link between these two deleterious conditions, is an important public health challenge, because of its high frequency and concomitant risk of cardiovascular and kidney diseases.[vi]
Our aim in this study was to evaluate the current evidence of the association between Obesity and DM. In this paper we discuss the relation between morbidly obese patients and their prevalence of having DM.
There is no simple solution to the epidemic of obesity. Its origin lies in our culture and society, and is epitomized by the suburban mall, with its drive-through fast-food restaurants.[vii] The primary treatment for obesity is dieting and physical exercise. To supplement this, or in case of failure, anti-obesity drugs may be taken to reduce appetite or inhibit fat absorption. In severe cases, surgery is performed or an intragastric balloon is placed to reduce stomach volume and/or bowel length, leading to earlier satiation and reduced ability to absorb nutrients from food.
[i] - Haslam DW, James WP (2005). "Obesity". Lancet 366 (9492): 1197–209. doi:10.1016/S0140-6736(05)67483-1. PMID 16198769.
[ii] Kushner, Robert (2007). Treatment of the Obese Patient (Contemporary Endocrinology). Totowa, NJ: Humana Press. pp. 158. ISBN 1-59745-400-1.
[iii] Adams JP, Murphy PG (July 2000). "Obesity in anaesthesia and intensive care". Br J Anaesth 85 (1): 91–108. doi:10.1093/bja/85.1.91. PMID 10927998
[iv] Obesity Issues for the Gastroenterologist, David A Johnson, MD, FACG, FACP. Posted: 10/15/2003; Updated: 10/31/2003.medscape.com/viewarticle/462995
[v] Obesity and hypertension. G Ital Cardiol (Rome).  2008; 9(4 Suppl 1):54S-59S (ISSN: 1827-6806)
[vi] Obesity and Hypertension: A Growing Problem. Thomas G. Pickering, MD, DPhil, Mt. Sinai School of Medicine, New York, NY. Posted: 07/01/2001; © 2001 Le Jacq Communications, Inc.
[vii]  Imaz I, Martínez-Cervell C, García-Alvarez EE, Sendra-Gutiérrez JM, González-Enríquez J (July 2008). "Safety and effectiveness of the intragastric balloon for obesity. A meta-analysis". Obes Surg 18 (7): 841–6. doi:10.1007/s11695-007-9331-8. PMID 18459025.

Methods


It is a registry study; it recruited 198 morbidly obese patients who have undergone preoperative blood tests, liver ultrasound to prepare for surgery.
Different tests were done for preoperative assessment which includes blood tests e.g. Hb Level, blood sugar, TG, SGOT, SGPT, GGT, alkaline phosphatase, serum albumin and bilirubin, T4, TSH and the levels of cortisone both in the morning and evening. Blood pressure is measured and liver ultrasound done.
Enrolled patients were evaluated to see the incidence of DM in obese patients.
The data was analyzed based on; Overall and DM (Diabetic and Non-Diabetic) to see if there is any significant difference between study groups.
Statistical Methodology
Frequency statistics (number, percent) were mainly calculated for all the measurements. Comparability was assessed using chi-square test for categorical variables, like sex, etc. and t-test for continuous variables, like age.

Discussion and Results


Insulin resistance in obesity is strictly related to the development of, IGT[i], hepatic steatosis, as well as to the combination of these factors, also known as metabolic syndrome[ii]. Furthermore, insulin resistance is associated with systemic inflammation, endothelial dysfunction, early atherosclerosis and disordered fibrinolysis. It is alarming that these metabolic and cardiovascular complications are already found in obese children and adolescents. The presence of these alterations in prepubertal children is then particularly worrying, as insulin resistance and related complications might be further exacerbated by the influence of puberty, due to the physiological decrease in insulin sensitivity associated with normal pubertal development[iii].
Obese children with a similar BMI can differ on the basis of the degree of insulin resistance in the risk for complications. In fact, those with a more impaired insulin sensitivity show, for example, a greater risk for type 2 diabetes mellitus (T2DM) and cardiovascular disease. It has also been clearly shown that insulin resistance in childhood can track in adult life. A recent study has shown that insulin resistance at the age of 13 years predicts insulin resistance at age 19, independently of BMI, and is also associated with cardiovascular risk in adulthood[iv].
Figure (1) shows the incidence of Diabetes and Fatty Liver in our sample.
As mentioned before, obesity is most commonly caused by a combination of excessive dietary calories and genetic susceptibility, although a few cases are caused solely by genes, endocrine disorders, medications or psychiatric illness.

Conclusion


Obesity may antedate and predict the development of hypertension. Even among subjects with normal or optimal blood pressure, the obese subjects are more likely to develop high blood pressure levels in the following years. The opposite can also be true. Hypertensive subjects are more likely to develop obesity than normotensive ones.

References


1. Haslam DW, James WP (2005)."Obesity" Lancet 366(9492): 1197–209. doi:10.1016/S0140-6736(05)67483-1. PMID 16198769.
2. Kushner, Robert (2007). Treatment of the Obese Patient (Contemporary Endocrinology). Totowa, NJ: Humana Press. pp. 158. ISBN 1-59745-400-1.
3. Adams JP, Murphy PG (July 2000). "Obesity in anaesthesia and intensive care". Br J Anaesth 85 (1): 91–108. doi:10.1093/bja/85.1.91. PMID 10927998. 4. Obesity Issues for the Gastroenterologist, David A Johnson, MD, FACG, FACP. Posted: 10/15/2003; Updated: 10/31/2003.medscape.com/viewarticle/462995.
5. Obesity and hypertension. G Ital Cardiol (Rome).  2008; 9(4 Suppl 1):54S-59S (ISSN: 1827-6806).
6. Obesity and Hypertension: A Growing Problem. Thomas G. Pickering, MD, DPhil, Mt. Sinai School of Medicine, New York, NY. Posted: 07/01/2001; © 2001 Le Jacq Communications, Inc.
7. Imaz I, Martínez-Cervell C, García-Alvarez EE, Sendra-Gutiérrez JM, González-Enríquez J (July 2008). "Safety and effectiveness of the intragastric balloon for obesity. A meta-analysis". Obes Surg 18 (7): 841–6. doi:10.1007/s11695-007-9331-8. PMID 18459025.
8. Sinha R, Fisch G, Teague B, Tamborlane WV, Banyas B, Allen K, Savoye M, Rieger V, Taksali S, Barbetta G, Sherwin RS & Caprio S. Prevalence of impaired glucose tolerance among children and adolescents with marked obesity. New England Journal of Medicine 2002; 346:802–810.
9. Eckel RH, Grundy SM & Zimmet PZ. The metabolic syndrome. Lancet 2005; 365:1415–1428.
10. Caprio S, Plewe G, Diamond MP, Simonson DC, Boulware SD, Sherwin RS & Tamborlane WV. Increased insulin secretion in puberty: a compensatory response to reductions in insulin sensitivity. Journal of Pediatrics 1989; 114:963–967.
11. Sinaiko AR, Steinberger J, Moran A, Hong CP, Prineas RJ & Jacobs DR Jr. Influence of insulin resistance and body mass index at age 13 on systolic blood pressure, triglycerides, and high-density lipoprotein cholesterol at age 19. Hypertension 2006; 48:730–736.
12. Hedley AA, Ogden CL, Johnson CL, Carroll MD, Curtin LR & Flegal KM. Prevalence of overweight and obesity among US children, adolescents, and adults, 1999–2002. Journal of the American Medical Association 2004; 291:2847–2850.
13. Bhargava SK, Sachdev HS, Fall CH, Osmond C, Lakshmy R, Barker DJ, Biswas SK, Ramji S, Prabhakaran D & Reddy KS. Relation of serial changes in childhood body-mass index to impaired glucose tolerance in young adulthood. New England Journal of Medicine 2004; 350:865–875.
14. Day C and Saksena S. Nonalcoholic steatohepatitis: definitions and pathogensis. J Gastroenterol Hepatol 17: S377–S384, 2002.
15. Srinivasan SR, Bao W, Wattigney WA, et al. Adolescent overweight is associated with adult overweight and related multiple cardiovascular risk factors: the Bogalusa Heart Study. Metabolism. 1996;45:235-240.

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