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INTRODUCTION
Type 2 diabetes, or non-insulin dependent diabetes mellitus (NIDDM), is a multifactorial disease characterized by mild to severe dysregulation of glucose homeostasis. Glucose, an essential nutrient, is the major source of energy in the human body. In healthy individuals, blood glucose concentrations are
effectively held within a relatively narrow range (between 80 and 100 mg/mL in the post-absorptive state) regardless of calorie intake. This is particularly important because, despite variations in the time and amount of food consumed, the glucose requirements of peripheral tissues, especially the central nervous system, are constant. The maintenance of such precise glucose homeostasis is dependent almost entirely upon
Presented in part at Ross Products Research Conference on Medical Issues, Synergy in Medical Nutritional Therapy, November 6 8, 2000, Key Largo, Florida. Address reprint requests to: Roger B. McDonald, PhD, Professor, Department of Nutrition, University of California, One Shields Ave, Davis, CA 95616-8669. E-mail: rbmcdonald@ucdavis.edu
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ETIOLOGY
The development of NIDDM was once thought to be the result of an endogenous, age related alteration in the ability of insulin to mediate uptake of glucose in peripheral tissues. This belief was based on the observation of a gradual but significant rise in insulin resistance with age independent of other variables. However, numerous studies have demonstrated that endogenous factors such as changes in insulin receptor number and affinity do not play a significant role in the development of NIDDM [5]. Also, the dramatic increase in the rate of diabetes among younger populations is evidence that NIDDM is not a disease of aging per se, but rather the consequence of modifiable, environmental factors. The two most important factors contributing to the development of NIDDM are obesity and physical inactivity. The prevalence of obesity in the U.S. population as a whole is about 20%, but it is even higher among certain non-Caucasian groups [6]. During the past decade, the percentage of Americans defined as obese (30 pounds over ideal weight) has increased by about 33%. It is not a coincidence that these figures mirror the dramatic rise in diabetes over the same 10-year period. The association between obesity and the incidence of NIDDM is very strong. The vast majority of recent studies in humans and rodents have demonstrated a positive relationship between obesity and insulin resistance [5,7]. Several cohort studies indicate that weight gain during adulthood, the degree of obesity, and the duration of obesity are all strong and independent risk factors for the development of NIDDM [8]. Decreased physical activity is becoming more common in the U.S. and throughout the world because of the decrease in demand for physical labor and an increase in sedentary occupations. Almost a third of the adult population in the U.S. does not participate in exercise or other physical activity [4]. This
BACKGROUND
NIDDM is increasingly common throughout the world. The World Health Organization has predicted that between 1997 and 2025, the number of diabetics will double from 143 million to about 300 million [1]. The incidence of NIDDM is highest in economically developed nations, particularly the U.S., where approximately 6.5% of the population (17 million people) have either diagnosed or undiagnosed diabetes. There are an additional 25 to 30 million people in the U.S. with impaired glucose tolerance. The incidence of NIDDM in the U.S. has increased by about 33% over the past decade and is expected to increase further. However, the greatest rise in the prevalence of NIDDM is projected to occur in developing countries, particularly India and China [2]. The prevalence of both NIDDM and glucose intolerance increases with age. It is estimated that between 25% and 30% of the U.S. population aged 65 and older has NIDDM or impaired glucose tolerance [3]. Older adults exhibiting no clinical signs of diabetes often demonstrate decreased glucose tolerance (i.e., decreased glucose disposal rate as determined by an oral glucose tolerance test). Although it is often considered a disease primarily of the elderly and middle-aged, diabetes has
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CONCLUSION
Type 2 diabetes is a chronic, progressive disease characterized by insulin resistance with an inadequate compensatory insulin secretory response. NIDDM is becoming increasingly common throughout much of the world, and the incidence of this disease is rising most rapidly among younger people. The reason for this dramatic increase in NIDDM is the increased prevalence of obesity and physical inactivity which are becoming more common in a world where physical labor is less necessary and calorie-dense foods are readily available. Proper diet and exercise can effectively prevent or reverse NIDDM in most cases, but patient compliance is difficult. Hypoglycemic agents are an important therapeutic option, especially for patients who do not respond to diet and exercise alone. Hyperglycemia, an inevitable consequence of NIDDM, is the source of most of the deleterious effects usually associated with this disease. High blood glucose concentrations promote auto-oxidation of glucose to form free radicals. The generation of free radicals beyond the scavenging abilities of endogenous
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ACKNOWLEDGMENTS
This work was supported, in part, by a gift from the California Age Research Institute.
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REFERENCES
1. World Health Organization: The World Health Report 1998. Life in the 21st Centurya Vision for All. Geneva: World Health Organization, 1998. 2. King H, Aubert RE, Herman WH: Global burden of diabetes 19952025. Prevalence, numerical estimates and projections. Diabetes Care 21:14141431, 1998. 3. Kenny SJ, Aubert RE, Geiss L: Prevalence and incidence of non-insulin-dependent diabetes. In: Harris MI (ed): Diabetes in America 2nd ed. Washington, DC: National Institute of Diabetes and Digestive and Kidney Diseases NIH publication, pp 4767, 1995. 4. Mokdad AH, Ford ES, Bowman BA, Nelson DE, Engelgau MM, Vinicor F, Marks JS: Diabetes trends in the U.S.: 19901998. Diabetes Care 23:12781283, 2000. 5. Ruhe RC, McDonald RB: Carbohydrate metabolism and aging. In Watson RR: Handbook of Nutrition in the Aged, 3rd ed. Boca Raton: CRC Press, pp 205237, 2000. 6. Flegal KM, Carroll MD, Kuczmarski RJ, Johnson CL: Overweight and obesity in the United States: prevalence and trends, 1960 1994. Int J Obes 22:3947, 1998. 7. Kelly GS: Insulin resistance: lifestyle and nutritional interventions. Alter Med Rev 5:10932, 2000. 8. Wannamethee SG, Shaper AG: Weight change and duration of overweight and obesity in the incidence of type 2 diabetes. Diabetes Care 22:12661272, 1999. 9. Heath GW, Gavin JR, Hinderliter JM, Hagberg JM, Bloomfield SA, Holloszy JO: Effects of exercise and lack of exercise on glucose tolerance and insulin sensitivity. J Appl Physiol 55:512 517, 1983. 10. Seidell JC: Time trends in obesity: an epidemiological perspective. Horm Metab Res 21:155158, 1998. 11. Resnick HE, Valsania P, Halter JB, Lin X: Relation of weight gain and weight loss on subsequent diabetes risk in overweight adults. J Epidem Comm Health 54:596602, 2000. 12. Cox JH, Cortright RN, Dohm GL, Houmard JA: Effect of aging on
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