3. الرؤية
تحقيق التميز فى مجال الصيدلة من خلال التعليم المبتكر و الممارسة المعاصرة و المساهمات العلمية القيمة

4. توفر كلية الصيدلة جامعة حورس تعليما صيدليا مثاليا لاعداد الخريجين القادرين على تقديم ممارسة صيدلية و رعاية صحية عالية الجودة للمجتمع و تحقيق مساهمات ذات مغزى للبحث العلمى

6. Biochemistry (2) - PB-334
This course includes:
Normal metabolic pathways of carbohydrates, lipids and proteins, as well as
Integration of metabolism during feeding and fasting cycle.
Metabolism in different organs.
Classification of hormones according to their mechanism of action are also described. Besides,
Assessment of disorders of plasma proteins, minerals, carbohydrates and lipid metabolism are discussed.

7. Course Code: PB- 334
Course Title: Biochemistry (2) CW P O F
Final Total
Quiz
Activity
Attendance
Total
P (1)
P(2)
Oral
Mid 5 15 10 25 40 50
100

8. Metabolism of carbohydrates(Sugars)
Metabolism is defined as the sum of chemical reactions that occur in the body(Metabolic pathways or Biochemical pathways).
Metabolic pathways or Biochemical pathways:
Catabolic. هدم
Anabolic. بناء

10. large complex molecules Carbohydrates (Sugars): Starch, glycogen
Fats (triglycerides)
Proteins
ATP
+ Heat
Building blocks:
Simple sugars:
(Glucose, fructose, Galactose)
Fatty acids and glycerol.
Amino acids.

11. CATABOLISM (CELLULAR RESPIRATION)
Breakdown of food in the presence of OXYGEN
MITOCHONDRION

13. ATP

14. LECTURE 1: DIGESTION & ABSORPTION OF CABOYDRATES

15. Complex carbohydrates :Starch - Glycogen
Complex carbohydrates :Starch - Glycogen. ( glucose units linked by  1,4 Glycosidic-linkages and  1,6 branches.

16. 2. Disaccharides:
lactose (milk sugar) = Glucose + Galactose.
Maltose(malt sugar) = Glucose+ Glucose.
Sucrose (cane sugar) = Glucose + Fructose.
3. Monosaccharides: Glucose, Fructose, Galactose.
4. Fibers: Cellulose (β-glucose units linked by β 1-4 Glycosidic linkages) ( not digested by humans):prevents constipation.

21. Digestion in the stomach: NO DIGESTION
Carbohydrate digestion stops temporarily in the stomach because the high acidity inactivates salivary α-amylase.
Digestion in the small intestine:
When the acidic stomach contents reach the small intestine, they are
neutralized by bicarbonate secreted by the pancreas, where, pancreatic α-
amylase continues the process of carbohydrate digestion.
Pancreatic amylase: completes the digestion of starch into maltose and isomaltose.
ᾳ-Amylase cannot cleave ᾳ (1-6) glycosidic bonds (branch points). Also, disaccharides are resistant to the action of α-amylase.

22. b. Intestinal disaccharidases:
The final digestive processes occur at the mucosal lining of the upper jejunum by the action of brush border enzymes (Disaccharidases):
The end products of carbohydrate digestion are mainly:
Glucose, Galactose and Fructose.

26. Absorption in Duodenum and upper jejunum.
Glucose and galactose:
Active process (needs ATP): Glucose can be absorbed against its concentration gradient.
Use Sodium dependent glucose co-transporter(SGLT1).
2. Fructose: sodium-independent facilitated diffusion using (GLUT5).
3. All sugars (Glucose, Galactose and Fructose) at the basal border are then transported from the intestinal mucosal cell into the portal circulation by facilitated diffusion using (GLUT2).

28. Lactose and Sucrose intolerance (Disaccharides intolerance)
Due to Di-saccharidase deficiency (Lactase & Sucrase deficiency)
Leads to:
Accumulation of undigested lactose and sucrose in the large intestine leading to:
Osmotic diarrhea: due to withdrawal of water from the intestinal mucosa to the intestinal lumen.
Flatulence, abdominal cramps:
Due to bacterial fermentation of lactose and sucrose into 2- and 3- carbon compounds (such as lactic acid) ,which are also osmotically active, with the release of large volumes of CO2 gas and H2 gas (can be measured in breath).

29. Hereditary deficiency of an individual “disaccharidases” in infants and children which is a rare condition e.g., congenital lactase deficiency (lactose intolerance) leading to failure to thrive when fed on breast milk or normal infant formula. The condition is treated by avoiding ingestion of lactose containing diets (Milk and dairy products). Also, inherited- sucrase deficiency (Sucrose intolerance).Treatment includes dietary restriction of sucrose.

30. 2. Age-dependent loss of lactase: (Lactose intolerance): In most human beings lactase activity begins to fall after weaning throughout adolescence and adulthood. Up to 90% of African and Asian adults are lactase deficient and therefore are less able to metabolize lactose than individuals from North European origin. Treatment for this disorder is to reduce consumption of milk and eat yogurt.

31. 3. Conditions leading to injury of the intestinal mucosa including: Intestinal diseases such as severe diarrhea and drugs that injur the mucosa of the small intestine. E.g., brush border enzymes are rapidly lost in normal individuals with severe diarrhea. So these patients cannot drink or eat significant amount of dairy products or sucrose without diarrhea.

32. Glucose transporters (GLUTs)
(GLUTs) are Protein carriers for glucose across cell membranes of different tissues

33. GLUT1
Tissues: Abundant in adults cell membranes of erythrocytes, endothelium of barrier tissues such as blood –brain-barrier, placenta and kidney and is also abundant in fetal tissues.
Function: Responsible for the low level of basal glucose uptake required to sustain energy generation in cells.
GLUT 2
Tissues: Liver, pancreatic β-cells, intestine and kidney.
Function: It is important for regulation of blood glucose levels due to their
presence in the two organs responsible for regulation of blood glucose
level;the pancreas and the liver.

34. GLUT2 in the β-pancreatic cells:
Has a high capacity but low affinity for glucose. When blood glucose level is high (hyperglycemia) there is rapid uptake of glucose into β- pancreatic cells this stimulates secretion of insulin by β-cells in order to lower blood glucose levels. (acts as glucose sensor in pancreas).
GLUT2 in the liver:
Has high capacity but low affinity for transporting glucose is important for the rapid uptake of elevated glucose levels in the portal blood after meals(to avoid hyperglycemia after meals).
GLUT-2 is responsible for the rapid release of glucose from hepatic cells to the blood stream in cases of hypoglycemia.

35. GLUT-3: GLUT-4 Tissues: Brain, kidney, placenta.
Function: GLUT-3 has high affinity for glucose allowing it to transport
even in times of low glucose concentrations.
GLUT-4
Tissues: in heart, skeletal muscles and adipose tissue.
Function: Insulin-stimulated uptake of glucose.
In these tissues insulin produces translocation of glucose transporters to
the outer cell membrane surface, therefore, increases the number of protein
carriers (transporters) of glucose and stimulates glucose uptake by these
tissues when the blood glucose is increased (hyperglycemia).

36. In absence of insulin the glucose transporters are endocytosed to form an intracellular pool and glucose uptake is reduced, which is an important mechanism to maintain blood glucose within normal level. The amount of GLUT-4 in the muscle cell membrane increases with endurance training.