Diabetes mellitus type II

Diabetes mellitus type II

Type II diabetes mellitus is caused by a misbalance between β-cell function and insulin resistance (1). Insulin levels can be normal or elevated. Type II patients develop hyperglycemia, because insulin secretion does not fully compensate for insulin resistance (2). They do not show ketoacidosis, because they secrete enough insulin to prevent the conversion of fatty acids to ketoacids. Treatment consists of weight loss and caloric restriction. Usually this does not help appropriately and drugs have to be used to decrease glucose uptake, increase insulin secretion and to decrease insulin resistance.

In DM type II patients, the physiology by the GLP-1 regulation is clearly disturbed, as shown in the graphic below. These patients mostly have a larger food intake (1). The postprandial incretin GLP-1 response is diminished (2). The insufficient GLP-1 concentration in the blood has several unwanted effects: the β-cells in the pancreas release less insulin (3), the glucagon release by the α-cells is less inhibited (4), the gastric emptying is not delayed (5), the appetite remains (6) and the dipeptidyl peptidase 4 (DPP-IV) enzyme is overactivated (7). All these events results in postprandial hyperglycemia (8).


I. Type 2 diabetes mellitus is associated with hypertension and dyslipidemia.

II. Obese persons have a high incidence for type 2 diabetes type.


A patient has been extremely thirsty. She complains of polyuria (4-5L/day) and polydipsia. Which two disorders could produce these symptoms?