Progressive failure of pancreatic beta cells

Diabetes Concept

Concept Map: Type 2 Diabetes Mellitus

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Risk Factors:

Weight, Race,

Inactivity, Family history,

Fat distribution, Age


Execrise, Eating habits,

Regular checkups


Glycated hemoglobin

(A1C) test

Random or fasting blood sugar test

Oral glucose tolerance test

Structural Changes:

Potential brain structure changes

Myocardial degradation

Circulation changes

Possible amputation

Pancreatic changes

Signs and Symptoms:

Increased thrist, Frequent

urination, Increased hunger,

Weight loss, Fatigue, Blurred

vision, Frequent infections,

Sores/slow healing, Darker skin


If untreated: Heart disease,

Stroke, Kidney disease,

Dialysis, Blindness,



Blood sugar monitoring, Exercise,

Healthy eating habits,

Possible medications / insulin therapy

Functional Chnages:

Chnages to kidney function, Changes to pancreas function,

Pancreatic Changes

There are some pancreatic changes that have been associated with the onset of Type 2 Diabetes Mellitus, especially the progressive failure of pancreatic beta-cells apparently as a response to insulin resistance and leading to under-production and a loss of pancreatic function (Feinglos & Bethel, 2008; Serrano, 2009). Type 2 Diabetes Mellitus can have a circular effect on the pancreas; though it is typically a structural and/or functional degradation in the pancreas that brings on Type 2 (as well as Type 1) Diabetes Mellitus, the start of the disease can lead to further degradation of pancreatic structure and function in a circular pattern that will increase insulin resistance and reduce insulin production by breaking down the cascading cycle of insulin production and consumption that occurs in the healthy body (Fineglos & Bethel, 2008; Levene & Donnelly, 2011). The production of glucagon, another hormone that, put simply, counters the effects of insulin and has opposing effects on the body by forcing stored glucose into the bloodstream and raising blood sugar levels, addressing some of the complications that can occur in Type 2 Diabetes Mellitus as the insulin is both resisted in the body’s cells and as production decreases in the pancreas (Leven & Donnelly, 2011). This is not something that occurs in all cases of Type 2 Diabetes Mellitus, and congenital pancreatic degradation is almost always a causal element of Type 1 Diabetes Mellitus, but pancreatic damage can occur as the result of complications of Type 2 Diabetes Mellitus when it remains untreated or is diagnosed too late (Fineglos & Bethel, 2008; Serrano, 2009; Levene & Donnelly, 2011).

The pancreatic beta-cells that are directly involved in the production of insulin are located in the Islets of Langerhans, in a specific area of the pancreas that can suffer from severe structural damage and change during the course of Type 2 Diabetes Mellitus as well as in Type 1 Diabetes Mellitus; as this structural change occurs it further degrades the functional capabilities of the pancreas and thus exacerbates the self-propelling cycle of insulin resistance and a lack of insulin production still further (Feinglos & Bethel, 2008; Serrano, 2009). Again, this is not always a result of Type 2 Diabetes Mellitus, and pancreatic degradation is more commonly associated with the onset of Type 1 Diabetes Mellitus, however if Type 2 Diabetes Mellitus progresses far enough the pancreatic degradation will result in similar consequences and insulin therapy might eventually be required (Feinglos & Bethel, 2008; Levene & Donnelly, 2011). As with any disease brought about by and/or causing tissue degradation without a foreign agent’s presence, allowing progression of Type 2 Diabetes Mellitus will increase the degradation of pancreatic tissue and continue to exacerbate the disease (Levene & Donnelly, 2011). As the Islets of Langerhans continues to structurally degrade, the functionality of the pancreas degrades and the body’s ability to produce and process insulin and so regulate blood sugar levels and maintain proper metabolic processes, eventually resulting in the terminal stages of the disease (Feinglos & Bethel, 2008; Levene & Donnelly, 2011).

Risk Factors

Being overweight, specifically long-term morbid obesity, is one of the most common and extreme risk factors for Type 2 Diabetes Mellitus (Levene & Donnelly, 2011). This is due to the relationship between the proportion of fatty tissue in the body and the level of insulin resistance the body’s cells demonstrate; the greater the fatty tissue deposits — especially in certain areas of the body — the greater the resistance to insulin becomes, and this triggers a cycle of reduced insulin production, growing resistance, etc. until the disease reached its full stage (Feinglos & Bethel, 2008; Levene & Donnelly, 2011). Controlling weight is thus one of the primary means of prevention and of controlling or stopping the progression — in some cases even reversing — Type 2 Diabetes Mellitus (Levene & Donnelly, 2011).

A lack of physical activity and regular exercise is also a significant risk factor in the development of Type 2 Diabetes Mellitus for several reasons. Not only does exercise help to control weight and so help to prevent and control the disease as described above, but regular exercise also helps the body to burn glucose, removing it from the bloodstream and allowing insulin to function properly, and it also increases the sensitivity of body cells to insulin (Levene & Donnelly, 2011). The greater degree of sensitivity to insulin by the body’s cells makes the resistance to insulin less likely to occur, and thus the disease as a whole is less likely to develop when regular exercise occurs even in overweight and obese individuals (Levene & Donnelly, 2011). Again, this is a very effective way to prevent and control the disease.


Feinglos, M. & Bethel, M. (2008). Type 2 Diabetes Mellitus. New York: Springer.

Levene, S. & Donnelly, R. (2011). Management of Type 2 Diabetes Mellitus. New York: Elsevier.

Serrano, M. (2009). Type 2 Diabetes Mellitus. New York: Elsevier.

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