<s>[INST] context: The hormone glucagon stimulates ketogenesis whereas insulin inhibits.The increased ratio of glucagons/insulin in diabetes mellitus promotes ketone bodies formationDiabetic ketoacidosisIt arises because of a lack of insulin in the body.The lack of insulin and corresponding elevation of glucagon leads to increased release of glucose by the liver (a process that is normally suppressed by insulin) from glycogen and through gluconeogenesis.High glucose levels spill over into the urine, taking water and solutes (such as sodium and potassium) along with it in a process of osmotic diuresis.Ketones, too, paicipate in osmotic diuresis and lead to fuher electrolyte losses.This leads to polyuria, dehydration, and compensatory thirst and polydipsia.The absence of insulin also leads to the release of free fatty acids from adipose tissue, which are conveed, again in the liver, into ketone bodies (acetoacetate and beta-hydroxybutyrate).Beta-Hydroxybutyrate can serve as an energy source in absence of insulin-mediated glucose delivery, and is a protective mechanism in case of starvation.The ketone bodies, however, have a low pH and therefore turn the blood acidic (metabolic acidosis).The body initially buffers the change with the bicarbonate buffering system, but this system is quickly overwhelmed and other mechanisms compensate for the acidosis.One such mechanism is hyperventilation to lower the blood carbon dioxide levels (a form of compensatory respiratory alkalosis).This hyperventilation, in its extreme form, may be observed as Kussmaul respiration.Blood sugars rise, dehydration ensues, and resistance to the normal effects of insulin increases fuher by way of a vicious circle.As a result of the above mechanisms, the average adult DKA patient has a total body water shoage of about 6 liters (or 100 mL/ kg), in addition to substantial shoages in sodium, potassium, chloride, phosphate, magnesium and calcium.Glucose levels usually exceed 13.8 mmol/L or 250 mg/ dLBeta-hydroxybutyrate, despite chemically not actually being a ketone, is the principal "ketone body" in diabetic ketoacidosis.DKA is cmmon in type 1 diabetes as this form of diabetes is associated with an absolute lack of insulin production by the islets of Langerhans.In type 2 diabetes, insulin production is present but is insufficient to meet the body's requirements as a result of end-organ insulin resistance.Usually, these amounts of insulin are sufficient to suppress ketogenesis.If DKA occurs in type 2 diabetics, their condition is called "ketosis-prone type 2 diabetes".The clinical state of DKA is associated, in addition to the above, with the release of various counterregulatory hormones such as glucagon and adrenaline as well as cytokinesCerebral edema is the most dangerous DKA complication.It is more likely in those with more severe DKA, and in the first episode of DKA.Other factors in the development of cerebral edema are dehydration, acidosis and low carbon dioxide levels [/INST] question: Starvation and Diabetes Mellitus can lead on to ketosis. Which of the following features is in our of ketosis due to diabetes mellitus? | options: A: Increase in Glucagon/ Insulin ration, increased cAMP and increased blood glucose B: Decreased insulin, increased free fatty acid which is equivalent to blood glucose C: Decreased insulin, increased free fatty acid which is not equivalent to blood glucose D: Elevated insulin and free fatty acid, equivalent to blood glucose | answer: A </s>