Type 2 diabetes mellitus is best described as:

Type 2 diabetes mellitus is primarily characterized by insulin resistance, which is a situation where the body's tissues, such as muscle and adipose tissue, do not respond adequately to insulin. This impaired response causes the pancreas to produce more insulin to maintain normal blood glucose levels, leading to hyperinsulinemia initially. Over time, the pancreatic beta cells may become exhausted and unable to produce sufficient insulin, resulting in elevated blood glucose levels.

Insulin resistance is a key factor in the development of Type 2 diabetes and is often associated with other conditions such as obesity, sedentary lifestyle, and metabolic syndrome. Thus, describing Type 2 diabetes mellitus as "resistance to insulin by insulin-sensitive tissues" accurately captures the pathophysiological basis of the disease.

Additionally, Type 2 diabetes does not typically involve the autoimmune destruction of beta cells, as seen in Type 1 diabetes, nor does it necessitate the use of rapid-acting insulins like lispro over regular insulin as a defining characteristic. While glucagon secretion may indeed be influenced in Type 2 diabetes, it is not the primary mechanism that differentiates this condition. Therefore, stating that Type 2 diabetes is characterized by insulin resistance in insulin-sensitive tissues provides the clearest