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Carbohydrates are the preferred source of energy for the body.

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).

Structure of ATP: Adenosine Triphosphate


High-energy bonds

A
Adenosine

P
Phosphate groups

CATABOLISM: Molecule Breakdown


C6H12O6
Glucose is broken down into many molecules of ATP (higher # if O2 present)

A
Adenosine Diphosphate

When bond is broken, energy is released to do cellular work

The process of glucose metabolism involves

Glycolysis The citric acid cycle (Krebs cycle) Electron transport.

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.

Excess glucose is preferentially stored as glycogen BUT

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.

Consists of 3 types: 1) Type 1 diabetes 2) Type 2 diabetes 3) Gestational diabetes

Complications :

- Stroke - Heart attack - Kidney disease - Eye Disease - Nerve Damage

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

Insulin Glucagon Somatostatin Pancreatic Polypeptide Amylin

Insulin affects many organs:

It stimulates skeletal muscle fibers. It stimulates liver cells.

amino acids uptake

protein synthesis

It acts on fat cells


It inhibits production of certain enzyme. In each case, insulin triggers these effects by binding to the insulin receptor.

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!