von Dr. Sankarganesh Jeyaraj
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| 1. INTRODUCTION
1.1. Diabetes Mellitus Human bodies need to maintain a glucose concentration level in a narrow range (70 - 109 mg/dl or 3.9 - 6.04 mmol/l). If the glucose concentration level is significantly out of the normal range (70 - 110 mg/dl), this person is considered to have hyperglycaemia (140 mg/dl or 7.8 mmol/l after an oral glucose tolerance test, or 100 mg/dl or 5.5 mmol/l after a fasting glucose tolerance test) or hypoglycaemia (less than 40 mg/dl or 2.2 mmol/l). Diabetes mellitus is a disease in the glucose-insulin endocrine metabolic regulatory system, in which the pancreas either does not release insulin or does not properly use insulin to uptake glucose in the plasma (1) (2) which is referred as hyperglycaemia. The consequences are that the body does not metabolize the glucose and builds up hyperglycaemia which eventually damages the regulatory system. Complications of diabetes mellitus include retinopathy, nephropathy, peripheral neuropathy and blindness (3). Diabetes mellitus is one of the worst diseases with respect to size of the affected population. The world wide diabetics affected population is much higher, especially in underdeveloped countries. Diabetes mellitus is currently classified as type 1 or type 2 diabetes (2). Type 1 diabetes was previously called insulin-dependent diabetes mellitus (IDDM) or juvenile-onset diabetes. It develops when the body’s immune system destroys pancreatic beta cells, the only cells in the body that synthesize the hormone insulin, which regulates blood glucose. This form of diabetes usually strikes children and young adults, although disease onset can occur at any age. Type 1 diabetes may account for 5% to 10% of all diagnosed cases of diabetes. Risk factors for type 1 diabetes include autoimmune, genetic, and environmental factors. Type 2 diabetes is adult onset or non-insulin-dependent diabetes mellitus (NIDDM) as this is due to a deficit in the mass of β cells, reduced insulin secretion (4), and resistance to the action of insulin. The relative contribution and interaction of these defects in the pathogenesis of this disease remains to be clarified (5). About 90% to 95% of all diabetics diagnose type 2 diabetes. Type 2 diabetes is associated with older age, obesity, family history of diabetes, prior history of gestational diabetes, impaired glucose tolerance, physical inactivity, and race/ethnicity. African Americans, Hispanic/Latino Americans, native Americans, some Asian Americans, native Hawaiian, and other Pacific Islanders are at particularly high risk for type 2 diabetes. Type 2 diabetes is increasingly being diagnosed [in children and adolescents.] 1. Topp,B, Promislow,K, deVries,G, Miura,RM, Finegood,DT: A model of beta-cell mass, insulin, and glucose kinetics: pathways to diabetes. J.Theor.Biol. 206:605-619, 2000 2. Bergman,RN, Ider,YZ, Bowden,CR, Cobelli,C: Quantitative estimation of insulin sensitivity. Am.J.Physiol 236:E667-E677, 1979 3. Derouich,M, Boutayeb,A: The effect of physical exercise on the dynamics of glucose and insulin. J.Biomech. 35:911-917, 2002 4. Kloppel,G, Lohr,M, Habich,K, Oberholzer,M, Heitz,PU: Islet pathology and the pathogenesis of type 1 and type 2 diabetes mellitus revisited. Surv.Synth.Pathol.Res. 4:110-125, 1985 5. Cerasi,E: Insulin deficiency and insulin resistance in the pathogenesis of NIDDM: is a divorce possible? Diabetologia 38:992-997, 1995 |
[Page 1]
CHAPTER 1 Introduction and Physiological Background 1. Diabetes Mellitus Human bodies need to maintain a glucose concentration level in a narrow range (70 - 109 ml/dl or 3.9 - 6.04 mmol/l). If one’s glucose concentration level is significantly out of the normal range (70 - 110 ml/dl), this person is considered to have a the plasma glucose problem: hyperglycemia (≥140 mg/dl or 7.8 mmol/l after an Oral Glucose Tolerance Test, or ≥100 mg/dl or 5.5 mmol/l after a Fasting Glucose Tolerance Test) or hypoglycemia (less than 40 mg/dl or 2.2 mmol/l) ([89], [96]). Diabetes mellitus is a disease in the glucose-insulin endocrine metabolic regulatory system, in which the pancreas either does not release insulin or does not properly use insulin to uptake glucose in the plasma ([9], [85]), which is referred as hyperglycemia. The consequences are that the body does not metabolize the glucose and builds up hyperglycemia which eventually damages the regulatory system. Complications of diabetes mellitus include retinopathy, nephropathy, peripheral neuropathy and blindness ([25]). Diabetes mellitus is one of the worst diseases with respect to size of the affected population. [...] [Page 2] [...] The world wide diabetics population is much higher, especially in underdeveloped countries. Diabetes mellitus is currently classified as type 1 diabetes or type 2 diabetes ([9], [85]). Type 1 diabetes was previously called insulin-dependent diabetes mellitus (IDDM) or juvenile-onset diabetes. It develops when the body’s immune system destroys pancreatic beta cells, the only cells in the body that make the hormone insulin, which regulates blood glucose. This form of diabetes usually strikes children and young adults, although disease onset can occur at any age. Type 1 diabetes may account for 5% to 10% of all diagnosed cases of diabetes. Risk factors for type 1 diabetes include autoimmune, genetic, and environmental factors. Type 2 diabetes is adult onset or non-insulin-dependent diabetes mellitus (NIDDM) as this is due to a deficit in the mass of β cells, reduced insulin secretion [53], and resistance to the action of insulin [32]. The relative contribution and interaction of these defects in the pathogenesis of this disease remains to be clarified [17]. About 90% to 95% of all diabetics diagnose type 2 diabetes. Type 2 diabetes is associated with older age, obesity, family history of diabetes, prior history of gestational diabetes, impaired glucose tolerance, physical inactivity, and race/ethnicity. African Americans, Hispanic/Latino Americans, Native Americans, some Asian Americans, Native Hawaiian, and other Pacific Islanders are at particularly high risk for type 2 diabetes. Type 2 diabetes is increasingly being diagnosed in children and adolescents ([93]). [9] R. N. Bergman, D. T. Finegood, S. E. Kahn, The evolution of beta-cell dysfunction and insulin resistance in type 2 diabetes, Eur. J. Clin. Invest., 32 (2002), (Suppl. 3), 35–45. [10] R. N. Bergman, Y. Z. Ider, C. R. Bowden and C. Cobelli, Quantitative estimation of insulin sensitivity, Am. J. Physiol., 236 (1979), E667–E677. [17] E. Cerasi, Insulin deficiency and insulin resistance in the pathogenesis of NIDDM: is a dovorce Possible?, Diabetologia 38, 992–997. [25] M. Derouich, A. Boutayeb, The effect of physical exercise on the dynamics of glucose and insulin, J. Biomechanics, 35 (2002), 911–917. [32] The report of the Expert Committee on the diagnosis and classification of diabetes mellitus, Diabetes Care, 20 (1997), 1183–1197. [53] G. Kloppel, M. Lohr, K. Habich, M. Oberholzer and P. U. Heitz, Islet pathology and the pathogenesis of type 1 and type 2 diabetes mellitus revisited, Surv. Synth. Path. Res. 4, 110–125. [85] B. Topp, K. Promislow, G. De Vries, R. M. Miura and D. T. Finegood, A Model of β-cell mass, insulin, and glucose kinetics: pathways to diabetes, J. Theor. Biol. 206 (2000), 605–619. [89] http://arbl.cvmbs.colostate.edu/hbooks /pathphys/endocrine/pancreas/index.html |
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