Diabetes mellitus, a group of syndromes with varying characteristics, is characterized by an increase in fasting blood glucose due to a deficiency of insulin. This condition is responsible for several complications such as blindness, amputation, renal failure, nerve damage, heart attacks, and stroke. Diabetes can be divided into two types: type 1 (T1D) and type 2 (T2D). T1D, which accounts for approximately 10% of diabetes cases in the United States, occurs when the body's immune system mistakenly attacks the pancreatic β cells, resulting in a complete lack of insulin. Environmental factors, like viral infections, and genetic determinants play a role in this destructive process. T1D leads to hyperglycemia, diabetic ketoacidosis (DKA), and hypertriacylglycerolemia due to the insulin deficiency. Individuals with T1D need to rely on externally administered insulin to manage their blood glucose levels and prevent complications. T2D, on the other hand, has a significant genetic component and arises from a combination of insulin resistance and dysfunctional β cells. Insulin resistance refers to the reduced ability of target tissues, including the liver, white adipose tissue, and skeletal muscle, to respond effectively to normal or elevated levels of insulin. While obesity is a common cause of insulin resistance, not all obese individuals develop diabetes. In the absence of β-cell dysfunction, obese individuals without diabetes can compensate for insulin resistance by producing higher amounts of insulin. However, T2D only occurs in individuals who are both insulin resistant and have impaired β-cell function. The metabolic changes observed in T2D are milder compared to the insulin-dependent form of the disease. This is because the inadequate insulin secretion in T2D still helps prevent severe ketone production and the onset of DKA. Current treatments for diabetes aim to control hyperglycemia but do not completely restore normal metabolic function. Prolonged elevation of blood glucose levels is associated with chronic complications such as cardiovascular disease, stroke, retinopathy, nephropathy, and neuropathy. 

Moving on to the questions:
5.1. Three patients undergoing evaluation for gestational diabetes are given an oral glucose tolerance test. Based on the provided data, patient #2 is considered prediabetic. While patient #1 and patient #3 have normal fasting blood glucose (FBG) and glucose tolerance (GT) levels, patient #2 exhibits impaired glucose tolerance at 2 hours, indicating prediabetes.
5.2. If there is a relative or absolute lack of insulin in humans, the liver would respond by increasing the production of 3-hydroxybutyrate, a ketone body. Low insulin levels promote the liver's synthesis of ketone bodies, utilizing acetyl coenzyme A generated through the β-oxidation of fatty acids supplied by hormone-sensitive lipase (HSL) in adipose tissue (not the liver). In addition, low insulin levels result in the activation of HSL, reduced glycogen synthesis, and increased gluconeogenesis and glycogenolysis.
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 (Fig. 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). T1D constitutes ~10% of >29 million cases of diabetes in the United States. The disease is characterized by an absolute deficiency of insulin caused by an autoimmune attack on the pancreatic β cells. This destruction requires an environmental stimulus (such as a viral infection) and a genetic determinant that causes the β cell to be mistakenly identified as “nonself.” The metabolic abnormalities of T1D include hyperglycemia, diabetic ketoacidosis (DKA), and hypertriacylglycerolemia that result from a deficiency of insulin. Those with T1D 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, white adipose, and skeletal 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 develop diabetes. In the absence of a defect in β-cell function, obese individuals without diabetes 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 acute 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 DKA. 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 cardiovascular disease and stroke (macrovascular) as well as retinopathy, nephropathy, and neuropathy (microvascular).
Choose the ONE best answer.
5.1. 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 has diabetes.
5.2. 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 hormone-sensitive lipase (HSL) in adipose tissue (not liver). Low insulin also causes activation of HSL, decreased glycogen synthesis, and increased gluconeogenesis and glycogenolysis.