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Final products of carbohydrate digestion in the digestive tract are monosaccharides (glucose [80%], fructose and galactose) Much of fructose and all galactose are converted to glucose in the liver and released back into the blood. Glucose is a large molecule that must be broken down into a form of energy usable by the cell (ATP).
A
Adenosine
P
Phosphate groups
A
Adenosine Diphosphate
Only 40% of the energy released through catabolism of glucose is captured in ATP. The remaining 60% escapes as heat that warms the interior of the cells and the surrounding tissues. If cells have inadequate amounts of glucose to catabolize, the immediately shift to the catabolism of fats for energy. In starvation, proteins are used for energy after carbohydrate and fats are depleted.
Only enough ATP for immediate cellular requirements is made at any one time Glucose that is NOT needed for ATP is ANABOLIZED into glycogen and stored for later use in the liver and in muscles. GLYCOGENESIS: synthesis of glycogen from glucose molecules Insulin stimulates glycogenesis (glycogen anabolism) inhibits glycogenolysis (glycogen catabolism)
Glucose is in liquid form. As the number of glucose molecules increases, the pressure inside the cell increases.
Converting glucose to glycogen (in solid form) relieves pressure inside the
cell.
When cells are saturated with glycogen (liver cells store 5 to 8% of their weight as glycogen, muscle cells 1 to 3%) additional glucose is converted to fat in the liver and stored as fat in adipose cells.
Without insulin, glucose transport into the cells will be insufficient. Lacking glucose, cells will have to rely on protein and fat catabolism for fuel.
Also, when there is not enough insulin, excess glucose cannot be stored in the liver and muscle tissue.
Instead,glucose accumulates in the blood-- above normal levels.
Hyperglycemia,
or High Blood Sugar.
Complications :
Type 1 Diabetes
- cells that produce insulin are destroyed - results in insulin dependence - commonly detected before 30
Type 2 Diabetes
- blood glucose levels rise due to 1) Lack of insulin production 2) Insufficient insulin action (resistant cells) - commonly detected after 40 - effects > 90% - eventually leads to -cell failure
(resulting in insulin dependence)
Gestational Diabetes
3-5% of pregnant women in the US develop gestational diabetes
In 1921, Dr. Frederick Banting discovered insulin, enabling people with diabetes to live long and healthy lives.
Consist of A & B chains linked by 2 disulfide bonds (plus additional disulfide in A) A = 21amino acids B = 30 amino acids
Produced within the pancreas by cells islets of Langerhans insulin mRNA is translated as a single chain precursor called preproinsulin removal of signal peptide during insertion into the endoplasmic reticulum generates proinsulin Within the endoplasmic reticulum, proinsulin is exposed to several specific endopeptidases which excise the C peptide, thereby generating the mature form of insulin Stored as granules
Zn
-Tyrosine Kinase receptors are the locks in which the insulin key fits - Involved in signal transduction (insulin hormone being1stmessenger)
Type 2 diabetes is frequently associated with obesity. Serum insulin levels are normal or elevated, so this is a disease of insulin resistance. A number of treatment options may be employed.
The bulk of the pancreas is an exocrine gland secreting pancreatic fluid into the duodenum after a meal. Inside the pancreas are millions of clusters of cells called islets of Langerhans. The islets are endocrine tissue containing four types of cells. In order of abundance, they are: beta cells, which secrete insulin and amylin; alpha cells, which secrete glucagon; delta cells, which secrete somatostatin gamma cells, which secrete a polypeptide.
Pancreatic Hormones
protein synthesis
glucose uptake
glycogen synthesis
fat synthesis
enzyme production
glycogen breaking
Biguanides:(Glucophage-metformin) lowers the production of glucose made in the liver Well accepted as the drug of first choice in Type II Major side effects are GI Lactic acidosis rare but serious side effect
Oldest of oral meds Until 1995 the only meds available 1st gen- Orinase,Tolinase,Diabinese 2nd gen-Glucotrol(glipizide), Micronase or Diabeta(glyburide) 3rd gen- Amaryl(glimeperide) Stimulate the pancreas to release more insulin, hypoglycemia can be side effect
Prandin(repaglinide) Starlix(nateglitinide) Stimulate insulin secretion when there is glucose present in the blood stream Used with meals
Precose(acarbose) Glyset(miglitol) Delay the conversion of carbohydrates into glucose during digestion Major side effect gas/bloating limits use
Avandia(rosiglitazone) Actos(pioglitazone) Sensitizes muscle and fat cells to accept insulin more easily FDA warning in May 2007 that Avandia may be associated with possibility of heart attacks or other CV events Cause or exacerbate CHF, watch closely for edema
Byetta(exenatide)-originally isolated from the saliva of Gila monster Lizard Shares several of the coregulatory effects of the incretin glucagon-like peptide-1(GLP-1) Improves glucose dependent insulin secretion Restores first phase insulin response Suppresses inappropriate glucagon secretion Slows rate of gastric emptying Increases satiety BID injection, main side effect nausea/weight loss
Dipepityl Peptidase 4 inhibitor-slows the inactivation of GLP-1 and GIP (glucose-dependent insulinotropic polypeptide) Januvia(sitagliptin) Very minimal side effects, weight neutral Most effective when used with metformin
Each type different onset, peak, and duration Rapid Acting:Novolog(aspart) Apidra(glulisine) Humalog(lispro) Onset-15 min Peak- 30-90 min Duration- 3-5 hrs Take at the beginning of meals
Humulin R and Novolin R (regular) Onset- 30-60 min Peak- 2-4 hrs Duration- 5-8 hrs Take 30 minutes before meals
Humulin N and Novolin N (NPH) Onset- 1-3 hrs Peak- 8 hrs Duration- 12-16 hrs Usually twice a day
Levemir (detemir) and Lantus (glargine) Also referred to as basal insulins Onset- 1 hr Peak- none Duration- 20-26hrs Usually once a day, may need bid as dose increases
Humulin 70/30 Novolin 70/30 Humulin 50/50 Onset 30-60 min Peak- variable Duration- 10-16 hrs Typically bid
Humalog Mix 75/25 and 50/50 Intermediate and rapid-acting Onset- 15min Peak- variable Duration- 10-16 hrs Typically bid
Novolog Mix 70/30 Intermediate and rapid-acting Onset- 15min Peak- variable Duration- 10-16 hrs
Think Diabetes- Who to screen! Good History and Physical Educate, educate, educate! Monitor Be aggressive- dont be afraid to use insulin!