>>> As described in the Fluid Mosaic Model, the plasma membrane is comprised of
“mosaic of components” namely phospholipids, cholesterol, proteins, and carbohydrates, all of
which contribute to the fluidity of the membrane. These molecules are continually moving,
as proposed by Singar and Nicolson, which enables the cell membrane to maintain its
function as a barrier between the inside and outside of the cellular environments.
Transport Method
Active/Passive
Material Transported
Diffusion
Passive
Small-molecular weight material
Osmosis
Passive
Water
Facilitated
transport/diffusion
Primary active transport
Passive
Sodium, Potassium, Calcium, Glucose
Active
Sodium, Potassium, Calcium
Secondary active
transport
Phagocytosis
Active
Amino Acids, Lactose
Active
Pinocytosis and
potocytosis
Receptor-mediated
endocytosis
Active
Large macromolecules, whole cells, or
cellular structures
Small molecules (liquids/water)
Active
Large quantities of macromolecules
>>> During the process of glycolysis, one molecule of glucose is broken down into two
molecules of pyruvate or lactate, two hydrogen ions, and two molecules of water. The "high
energy" intermediary molecules of ATP and NADH are created via catabolic pathway.
Subsequently, pyruvate molecules partake in the link reaction to produce acetyl-coA that
enters the TCA cycle.
>>> In anaerobic conditions by anaerobic glycolysis, two ATP molecules are formed in
which pyruvate is converted to lactate. While under aerobic conditions, a net synthesis of
32 ATP molecules are formed where pyruvate enters the citric acid cycle and proceeds
through oxidative phosphorylation.
>>> To break down glycogen in our body, we undergo glycogenolysis, the biological process
through which glycogen degrades into glucose and other small molecules. Glucagon and
insulin regulate glycogenolysis hormonally in reaction to blood sugar levels, while epinephrine
stimulates it during the fight-or-flight response. The release of usable glucose into the
bloodstream by the liver occurs because of glucagon's stimulation of this process.
>>> As the hormonal regulation of this pathway, glucagon increases glycogenolysis and
decreases glycogenesis in liver while insulin potently inhibits glycogenolysis in liver and muscle
and favors glycogenesis. Additionally, epinephrine nor epinephrine increase glycogenolysis in
the muscle and decrease glycogenesis.
>>> In the digestion of carbohydrates, the enzyme salivary amylase in the mouth
begins to break down starch into shorter polysaccharides then in the gastric juice
(stomach), salivary amylase is inactivated so no further carbohydrate digestion occurs. It
goes through the duodenum where pancreatic amylase acts on partly digested food
(endoglycosidase- a-amylase or amylopsin) converted into maltose, maltotriose,
oligosaccharides, and a-dextrin or limit dextrin. Lastly, in the small intestine where majority
of starch digestion and breakdown of disaccharides occur: the enzyme pancreatic amylase
breaks down starch into monosaccharides, disaccharides, and oligosaccharides.
>>> In the absorption of carbohydrates, monosaccharides are the main products of
dietary carbs digestion which are absorbed from jejunum in the small intestine into blood of
portal venous system and there are two ways to absorb these monosaccharides- facilitated
diffusion mediated by translocase for glucose, galactose and fructose and simple diffusion to
absorb mannose and xylose.
>>> Non-tropical Sprue. It occurs because of digestive proteases' activity on
oligopeptide gluten, which is produced from dietary oat, wheat, and rye. In those who are
sensitive, these poisonous peptides promote intestinal mucosal atrophy and inflammation
wherein the small intestine's capacity for absorption is impaired.
>>> Celiac Disease. Children develop it as an effect of oligopeptides originating from
wheat gluten being absorbed. Therefore, it is comparable to adult non-tropical sprue.
Symptoms of these diseases may disappear when gluten is cut out of the diet
>>> Hartnup Disease. It is a hereditary condition. It results from a malfunctioning
aromatic and hydrophobic amino acid carrier in the intestine. These amino acids are
therefore not absorbed. Due to a faulty kidney carrier, they are eliminated through the
urine.
>>> Chyluria or chylous fistula. It is due to abnormal connection between urinary tract
and lymphatics of small intestine which is characterized by milky urine excretion.
>>> Chylothorax. It is due to abnormal connection between pleural space of lungs and
lymphatics of small intestine in the affected person’s milky pleural fluid accumulation in
pleural space.
>>> Cholestasis. Cholestatic patients have liquid crystal vesicles formation instead of
mixed micelles. It is due to non-availability of adequate amounts of bile salts, phospholipids,
and cholesterol that lipid digestion and absorption is impaired in intra or extra hepatic
cholestasis.
>>> Essential Fatty Acid Deficiency (EFAD). It is due to malabsorption of lips which also
occurs in cholestatic patients. Since normal biliary secretion of phospholipid is required for
the creation of mixed micelles and chylomicrons, EFAD during cholestasis itself can hinder
effective lipid absorption and transport.