CLINICAL CORRELATES Decreased production of insulin, which is usually caused by autoimmune

destruction of pancreatic b cells, results in type 1 (formerly called insulindependent) diabetes mellitus.
Type 1 diabetes is characterized by hyperglycemia, the result of decreased uptake of glucose by cells and
increased output of glucose by the liver (due to low insulin and high glucagon levels in the blood). These
patients are dependent on exogenous insulin to survive.\

CLINICAL CORRELATES Намалено производство на инсулин, което обикновено се причинява от

автоимунно разрушаване на панкреатичните b клетки, води до тип 1 (преди това се нарича
инсулинзависим) захарен диабет. Диабет тип 1 се характеризира с хипергликемия, резултат от
намалено усвояване на глюкоза от клетките и повишена продукция на глюкоза в черния дроб
(поради ниските нива на инсулин и високо ниво на глюкагон в кръвта). Тези пациенти зависят от
екзогенния инсулин, за да оцелеят

Намалено освобождаване на инсулин от панкреаса или намалена чувствителност на тъканите към

инсулин (инсулинова резистентност) води до тип 2 (наричан преди това неинсулинозависим)
захарен диабет. Това състояние също се характеризира с хипергликемия.

(1) Glucose enters the pancreatic b cells via the insulin-independent glucose transporter, GLUT-2, which
stimulates release of preformed insulin and promotes the synthesis of new insulin. (2) Additionally,
amino acids (particularly arginine and leucine) cause the release of preformed insulin from b cells of the
pancreas, although to a lesser extent than that released by glucose.

(1) Глюкозата навлиза в клетките на панкреаса в чрез инсулин-независим глюкозен транспортер

GLUT-2, който стимулира освобождаването на предварително образуван инсулин и стимулира
синтеза на нов инсулин. (2) Освен това, аминокиселините (особено аргинин и левцин) причиняват
освобождаването на предварителнообразуван инсулин от клетките на панкреаса, въпреки че в по-
малка степен от тези, освободени от глюкоза.

b. Blood glucagon levels change depending on the content of the meal.

(1) A high-carbohydrate meal causes glucagon levels to decrease.

(2) A high-protein meal causes glucagon to increase (Figure 7-4).

(3) On a normal mixed diet, glucagon will remain relatively constant after a meal, while insulin increases.

C. Blood glucose levels during prolonged fasting (starvation) 1. Even after 5 to 6 weeks of starvation,
blood glucose levels are still in the range of 65 mg/dL. 2. Changes in fuel utilization by various tissues
prevent blood glucose levels from decreasing abruptly during prolonged fasting. 3. The levels of ketone
bodies rise in the blood, and the brain uses ketone bodies for energy, decreasing its utilization of blood
glucose. 4. The rate of gluconeogenesis and, therefore, of urea production by the liver decreases. 5.
Muscle protein is spared. Less muscle protein is used to provide amino acids for gluconeogenesis.

D. Blood glucose levels during exercise 1. During exercise, blood glucose is maintained by essentially the
same mechanisms that are used during fasting. 2. Use of endogenous fuels a. As the exercising muscle
contracts, ATP is used. b. ATP is regenerated initially from creatine phosphate. c. Muscle glycogen is
oxidized to produce ATP. AMP activates phosphorylase b, and Ca2+-calmodulin activates phosphorylase
kinase. The hormone epinephrine causes the production of cAMP, which stimulates glycogen
breakdown. 3. Use of fuels from the blood a. As blood flow to the exercising muscle increases, blood
glucose and fatty acids are taken up and oxidized by muscle. b. As blood glucose levels begin to decrease,
the liver, by the processes of glycogenolysis and gluconeogenesis, acts to maintain blood glucose levels