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Gangguan Metabolisme Karbohidrat
Gangguan Metabolisme Karbohidrat
METABOLISME KARBOHIDRAT
OVERVIEW DIABETES MELLITUS
INTRODUCTION
➢Diabetes mellitus (DM) → a group of metabolic disorders characterized by a chronic
hyperglycemic condition resulting from defects in insulin secretion, insulin action or
both.
➢DM is probably one of the oldest diseases known to man. It was first reported in
Egyptian manuscript about 3000 years ago.
➢ In 1936, the distinction between type 1 and type 2 DM was clearly made
OVERVIEW DIABETES MELLITUS
EPIDEMIOLOGY
• The worldwide prevalence of diabetes has continued to increase dramatically. Globally, as of 2011, an estimated 366 million
people had DM, with type 2 making up about 90% of the cases.
• The number of people with type 2 DM is increasing in every country with 80% of people with DM living in low- and middle-income
countries
OVERVIEW DIABETES MELLITUS
• A fundamental mechanism for the maintenance of glucose homeostasis is the rapid action of insulin to stimulate glucose
uptake and metabolism in peripheral tissues.
• Resistance to the actions of insulin in skeletal muscle is a major pathogenic factor in type 2 or type 1 diabetes mellitus
Insulin
Definitions and Concepts
Insulin → a peptide hormone secreted by the β
cells of the pancreatic islets of Langerhans and
maintains normal blood glucose levels by
facilitating cellular glucose uptake, regulating
carbohydrate, lipid and protein metabolism and
promoting cell division and growth.
Biosynthesis of
Insulin
Insulin is synthesized in the β cells of pancreas in the form of
preproinsulin → discharged into cisternal space of rough ER →
cleaved into proinsulin by proteolytic enzymes → Proinsulin with a
C-chain linking A & B chains then transported by microvesicles to
the Golgi apparatus → Proinsulin is released in vesicles →
maturing granules by prohormone converatse 2 & 3 and carboxy
peptidase → Insulin
Regulation and Mechanisms of Insulin Secretion at the Cellular Level
Synthesis and secretion of insulin is regulated by both nutrient and non-nutrient secretagogues
Nutrient secretagogues → Glucose → trigger insulin secretion from the β cell by increasing
intracellular ATP and closing of K+-ATP channels.
Brain
No effect
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