The aim of this paper is to review the information on type 1 and type 2 diabetes with emphasis on its etiology, pathogenesis and pathophysiology via literature review. Diabetes is a group of metabolic disorders characterized by a chronic hyperglycemic condition resulting from defects in insulin secretion, insulin action or both. Type 1 diabetes is the result of an autoimmune reaction to proteins of the islets cells of the pancreas while type 2 diabetes is caused by a combination of genetic factors related to impaired insulin secretion, insulin resistance and environmental factors such as obesity, overeating, lack of exercise and stress, as well as aging. The pathogenesis of selective β-cell destruction within the islet in type 1 diabetes mellitus is difficult to follow due to marked heterogeneity of the pancreatic lesions. At the onset of overt hyperglycemia, a mixture of pseudoatrophic islets with cells producing glycogen, somatostatin and pancreatic polypeptide, normal islets and islets containing both β-cells and infiltrating lymphocytes and monocytes may be seen. The autoimmune destruction of pancreatic β cells leads to a deficiency of insulin secretion that leads to the metabolic derangements associated with type 1 diabetes. The main pathophysiological features of type 2 diabetes are impaired insulin secretion and increased insulin resistance. The impairment of pancreatic β cell function notably shows progression overtime in type 2 diabetes although aging, obesity, insufficient energy consumption, alcohol drinking, smoking, etc are independent risk factors of pathogenesis of type 2 diabetes mellitus.   

	 

	Key words: Diabetes Mellitus, Pathophysiology, Pathogenesis, Etiology.

The pathogenesis and pathophysiology of type 1 and type 2 diabetes mellitus

Summary

Aims To assess mortality in patients with diabetes incident under the age of 30 years.



Methods A cohort of 23 752 diabetic patients diagnosed under the age of 30 years from throughout the United Kingdom was identified during 1972–93 and followed up to February 1997. Following notification of deaths during this period, age- and sex-specific mortality rates, attributable risks and standardized mortality rates were calculated.



Results The 23 752 patients contributed a total of 317 522 person-years of follow-up, an average of 13.4 years per subject. During follow-up 949 deaths occurred in patients between the ages of 1 and 84 years, 566 in males and 383 in females. All-cause mortality rates in the patients with diabetes exceeded those in the general population at all ages and within the cohort were higher for males than females at all ages except between 5 and 15 years. The relative risk of death (standardized mortality ratio, SMR), was higher for females than males at all ages, being 4.0 (95% CI 3.6–4.4) for females and 2.7 (2.5–2.9) for males overall, but reaching a peak of 5.7 (4.7–7.0) in females aged 20–29, and of 4.0 (3.1–5.0) in males aged 40–49. Attributable risks, or the excess deaths in persons with diabetes compared with the general population, increased with age in both sexes.



Conclusions This is the first study from the UK of young patients diagnosed with diabetes that is large enough to calculate detailed age-specific mortality rates. This study provides a baseline for further studies of mortality and change in mortality within the United Kingdom.

The British Diabetic Association Cohort Study, I: all-cause mortality in patients with insulin-treated diabetes mellitus.

Nearly 70 registries from more than 40 countries have collected and published incidence data of childhood Type 1 (insulin-dependent) diabetes mellitus up to the end of the 1980s. The majority of incidence data comes from regions of high incidence i. e. from Europe and North American. All these published data facilitate the descriptive comparison of incidence and variation of the occurrence of Type 1 diabetes roughly throughout the northern hemisphere. The aim of this paper is to review and compare the most recent epidemiology data on the incidence of Type 1 diabetes among children under the age of 15 years. A clear difference in incidence appeared between northern and southern hemisphere with no countries below the equator having an incidence greater than 15.0 per 100,000. In contrast above the equator the disease is common. Between continents the variation in incidence showed that the lowest incidences were found in Asia, followed by Oceania (Australia and New Zealand), South and North America, and the highest rates were in Europe. The incidence varied from 0.6 per 100,000 in Korea and Mexico to 35.3 per 100,000 in Finland showing prominent worldwide variation in incidence of Type 1 diabetes. The largest intracontinental variation in incidence appeared in Europe, varying from the highest in Finland to the lowest (4.6 per 100,000)_in northern Greece. The highest incidence in the world was in northern Europe, but within the continent scale there were some striking exceptions from the overall level of incidence. In Iceland, the northern-most island nation in Europe, the incidence is only one-half of that in Norway and Sweden and one-third of that in Finland. In contrast, in Sardinia in southern Europe the Type 1 diabetes incidence is virtually the same as in Finland, three times higher than overall incidence in Europe. Large variation was also seen in small “pockets” of countries, particularly in the Baltic sea region. The worldwide variation in incidence reflects the distribution of ethnic populations and demonstrates the importance of the differential genetic susceptibility between populations.

A review of the recent epidemiological data on the worldwide incidence of type 1 (insulin dependent) diabetes mellitus

The autoimmune disease process leading to childhood-onset type 1 diabetes appears to start in infancy, and decisions on treatment to prevent initiation of autoimmunity will need to be based on genetic susceptibility alone. We set out to quantify the absolute risk associated with human leukocyte antigen (HLA) DRB1-DQA1-DQB1 class II genotypes and to develop strategies for recruitment into primary prevention trials. HLA class II haplotype- and genotype-specific risks were derived from 753 United Kingdom families from the Bart's-Oxford population-based study of type 1 diabetes and combined with incidence data from the region to calculate the absolute risk of development of diabetes. A hierarchy of susceptibility was established for both HLA class II haplotypes and genotypes, and the sensitivity and specificity of each genotype was established relative to age at disease onset. Highest risk was conferred by the genotype DRB1*03-DQA1*0501-DQB1*0201/DRB1*0401-DQA1*0301-DQB1*0302 (5% absolute risk of diabetes by age 15 yr), although sensitivity was only 22.6%. Combining the six highest risk genotypes conferred similar risk but increased sensitivity to 36.6% and was most sensitive for diagnosis of diabetes before age 5 yr (48.4%), whereas inclusion of 11 genotypes achieved the same sensitivity for diagnosis for ages 10-14 yr. Analysis of genotype-specific risk should form the basis for design of future primary prevention trials in the general population.

/pdf/absolute-risk-of-childhood-onset-type-1-diabetes-defined-by-1oh4swwwus.pdf

Absolute Risk of Childhood-Onset Type 1 Diabetes Defined by Human Leukocyte Antigen Class II Genotype: A Population-Based Study in the United Kingdom

The incidence of diabetes mellitus by clinical type was determined for the community of Rochester, Minnesota, 1945–69. Overall adjusted incidence rates per 100,000 person-years were 8.4 for IDDM, 80.1 for obese NIDDM, 45.6 for nonobese NIDDM, and 3.6 for secondary diabetes, using our definitions. Strict use of National Diabetes Data Group criteria would have reduced the apparent incidence of all diabetes by about 20% through the deletion of NIDDM cases. The National Diabetes Data Group classification improved the clinical homogeneity of IDDM patients compared with “juvenile-onset” diabetes but had little effect on NIDDM relative to “maturity-onset” diabetes, since essentially the same patients were included in both groups. Separation of NIDDM into obese and nonobese subcategories accomplished little in the way of defining two more homogeneous subgroups.

Incidence of Diabetes Mellitus by Clinical Type

In November 1972 the British Diabetic Association sponsored a register to which notification was invited of all new cases of diabetes occurring in children aged 0-15 years in Great Britain and Ireland. More than 2000 cases were notified in the first two years. Notification suggested that there was a minimum yearly incidence of 7-67 cases per 100 000, though incidences varied from year to year and by geographical area. Several reports of simultaneous onset of diabetes in sibs of different ages provided evidence of clustering. A seasonal variation in incidence was found in children aged 5-15 years with peaks in the autumn and winter. The age distribution was bimodal with a main peak at about 11 years and a secondary peak at about 5 years. The sex ratio showed a male excess from 0-4 years and from 11-15 years and a female excess from 5-10 years. Overall there were slightly more male cases. Altogether 11% of patients had a first-degree relative with diabetes. The register and several investigations based on it will continue.

https://www.bmj.com/content/bmj/3/5983/580.full.pdf

Register of newly diagnosed diabetic children.

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Register of newly diagnosed diabetic children.