Chapter Summary, Questions Answers - Diabetes Mellitus

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Chapter: Biochemistry : Diabetes Mellitus

Diabetes mellitus is a heterogeneous group of syndromes characterized by an elevation of fasting blood glucose that is caused by a relative or absolute deficiency of insulin.


CHAPTER SUMMARY

Diabetes mellitus is a heterogeneous group of syndromes characterized by an elevation of fasting blood glucose that is caused by a relative or absolute deficiency of insulin (Figure 25.14). Diabetes is the leading cause of adult blindness and amputation and a major cause of renal failure, nerve damage, heart attacks, and stroke. Diabetes can be classified into two groups, type 1 (T1D) and type 2 (T2D). Type 1 diabetics constitute approximately 10% of the nearly 26 million diabetics in the United States. The disease is characterized by an absolute deficiency of insulin caused by an autoimmune attack on the β cells of the pancreas. This destruction requires a stimulus from the environment (such as a viral infection) and a genetic determinant that allows the β cell to be recognized as “nonself.” The metabolic abnormalities of T1D mellitus include hyperglycemia, ketoacidosis, and hypertriacylglycerolemia that result from a deficiency of insulin. Type 1 diabetics must rely on exogenous insulin delivered subcutaneously to control hyperglycemia and ketoacidosis. T2D has a strong genetic component. It results from a combination of insulin resistance and dysfunctional β cells. Insulin resistance is the decreased ability of target tissues, such as liver, adipose, and muscle, to respond properly to normal (or elevated) circulating concentrations of insulin. Obesity is the most common cause of insulin resistance. However, most people with obesity and insulin resistance do not become diabetic. In the absence of a defect in β-cell function, nondiabetic, obese individuals can compensate for insulin resistance with elevated levels of insulin. Insulin resistance alone will not lead to T2D. Rather, T2D develops in insulin-resistant individuals who also show impaired β-cell function. The metabolic alterations observed in T2D are milder than those described for the insulin-dependent form of the disease, in part, because insulin secretion in T2D, although inadequate, does restrain ketogenesis and blunts the development of diabetic ketoacidosis. Available treatments for diabetes moderate the hyperglycemia but fail to completely normalize metabolism. The long-standing elevation of blood glucose is associated with the chronic complications of diabetes including premature atherosclerosis (macrovascular) as well as retinopathy, nephropathy, and neuropathy (microvascular).


Figure 25.14 Key concept map for diabetes. GLUT = glucose transporter.

 
Study Questions
Choose the ONE best answer.

 

25.1 Three patients being evaluated for gestational diabetes are given an oral glucose tolerance test. Based on the data shown below, which patient is prediabetic?

A. Patient #1

B. Patient #2

C. Patient #3

D. None

Correct answer = B. Patient #2 has a normal fasting blood glucose (FBG) but an impaired glucose tolerance (GT) as reflected in her blood glucose level at 2 hours and, so, is described as prediabetic. Patient #1 has a normal FBG and GT, whereas Patient #3 is diabetic.

 

25.2 Relative or absolute lack of insulin in humans would result in which one of the following reactions in the liver?

A. Decreased activity of hormone-sensitive lipase

B. Decreased gluconeogenesis from lactate

C. Decreased glycogenolysis

D. Increased formation of 3-hydroxybutyrate

E. Increased glycogenesis

Correct answer = D. Low insulin levels favor the liver producing ketone bodies, using acetyl coenzyme A generated by β-oxidation of the fatty acids provided by adipose tissue. Low insulin also causes activation of hormone-sensitive lipase, decreased glycogen synthesis, and increased gluconeogenesis and glycogenolysis.

 

25.3 Which one of the following is characteristic of untreated diabetes regardless of the type?

A. Hyperglycemia

B. Ketoacidosis

C. Low levels of hemoglobin A1c

D. Normal levels of C-peptide

E. Obesity

F. Simple inheritance pattern

Correct answer = A. Elevated blood glucose occurs in type 1 diabetes (T1D) as a result of a lack of insulin. In type 2 diabetes (T2D), hyperglycemia is due to a defect in β-cell function and insulin resistance. The hyperglycemia results in elevated hemoglobin A1c levels. Ketoacidosis is rare in T2D, whereas obesity is rare in T1D. Connecting peptide is a measure of insulin synthesis. It would be virtually absent in T1D and initially increased then decreased in T2D. Both forms of the disease show complex genetics.

 

25.4 An obese individual with type 2 diabetes typically:

A. benefits from receiving insulin about 6 hours after a meal.

B. has a lower plasma level of glucagon than does a normal individual.

C. has a lower plasma level of insulin than does a normal individual early in the disease process.

D. shows improvement in glucose tolerance if body weight is reduced.

E. shows sudden onset of symptoms.

Correct answer = D. Most type 2 diabetics are obese, and almost all show some improvement in blood glucose with weight reduction. Symptoms usually develop gradually. These patients have elevated insulin levels and usually do not require insulin (certainly not 6 hours after a meal) until late in the disease. Glucagon levels are typically normal.

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