Carbohydrate Processes in Biochemistry

Carbohydrate Processes

• Glycogenesis - polymerizes glucose to form glycogen in the liver and skeletal muscle.
  • Occurs when glucose supply exceeds ATP demand.
  • Glucose is covalently bonded to form glycogen stores.
  • High ATP levels turn off glycolysis which allows for the formation of glycogen.
  • Formula: Glucose - Glucose 6 Phosphate - Glucose 1 Phosphate – Glycogen
• Glycogenolysis - hydrolyzes glycogen into glucose monomers in the liver and skeletal muscle.
  • Stimulated by low blood glucose levels.
  • Formula: Glycogen splits into Glucose 1 Phosphate - Glucose 6 Phosphate - Glucose.
    • Glucose is then used for energy.
    • Hepatocytes act as enzymes, converting Glucose 6 Phosphate to Glucose to allow diffusion into the bloodstream.
• Gluconeogenesis - forms glucose from noncarbohydrate precursors in the liver.
  • Occurs when dietary sources and glucose reserves are depleted.
  • Glucose is made from amino acids and glycerol.
  • Protects the nervous system against hypoglycemia by ensuring ongoing ATP synthesis.
  • Glucose uptake by brain cells is continuous while uptake by other body cells is regulated by insulin.

Lipid Processes

• Triglyceride absorption - chylomicrons transport triglycerides (fats) from the small intestine.
  • Chylomicrons are synthesized in intestinal epithelial cells.
  • The number of adipocytes remains constant except before puberty in children.
  • Lipemia is the presence of excess chylomicrons in blood plasma, giving it a milky appearance after a fatty meal.
  • Muscle cells and adipocytes remove triglycerides from chylomicrons in the bloodstream for 4-6 hours.
  • Adipose tissue is stored in subcutaneous areas, around kidneys and heart, within the abdomen, and in the breasts, hips, and buttocks.
• VLDL (very low-density lipoproteins) - formed when chylomicron remnants enter the liver and combine with proteins and synthesized triglycerides from lipogenesis.
  • VLDL are released back into the blood.
  • As triglycerides are released, the density of lipoproteins increases and VLDL transform into LDL.
• LDL (low-density lipoproteins) - mainly contain cholesterol and are taken up by cells through receptor-mediated endocytosis.
• HDL (high-density lipoproteins) - produced and released by the liver.
  • They pick up excess cholesterol and phospholipids from tissues and transport them to the liver.

Protein Processes

• Deamination - amino acids are converted into keto acids in the liver.
  • Ammonia is produced as a byproduct and converted to urea in the liver to be excreted by the kidneys.
  • Keto acids enter the citric acid cycle for energy production.
  • Excess amino acids are used for cellular respiration, but they must be modified in the liver first.
• Other protein functions:
  • Structural integrity of muscles, tendons, and ligaments.
  • Enzymatic activity.
  • Hormonal regulation.
  • Neurotransmitter synthesis.
  • Cell receptors.
  • Antibodies and cell membrane transport proteins.

Metabolic Balance

• Catabolism - breakdown of complex molecules into simpler ones, releasing energy (fueling cellular respiration).
• Anabolism - synthesis of complex molecules from simpler ones, requiring energy.
  • The rate of anabolism exceeds catabolism during embryonic and fetal development, infancy, and childhood to support growth and development.
  • An excess of anabolic processes over catabolism leads to weight gain.
• Nutrient pools - the body's current stock of available amino acids, carbs, and lipids.
  • The body manages these pools to maintain an adequate supply of nutrients for anabolic processes and energy.
• Organs involved in managing nutrient pools:
  • Liver: stores glycogen and performs key metabolic reactions.
  • Adipose tissue: stores triglycerides.
  • Skeletal muscle: stores glycogen and is abundant in protein.

Metabolic States

• Absorptive (fed state) - nutrients enter the bloodstream from the GI tract during and shortly after eating.
• Post-absorptive (fasted state) - the GI tract is empty and energy is supplied by the breakdown of body reserves.
  • The body must maintain an adequate nutrient supply regardless of whether it is in a fed or a fasted state.

Post-Absorptive (Fasted) State

• Post- absorptive state goals:
  • Maintain blood glucose levels within a normal range.
  • Provide energy to the brain and other tissues.
  • Preserve lean body mass.
• What happens at the end of the absorptive state:
  • GI tract is empty.
  • Blood glucose levels begin to decline.
  • Hormonal changes occur (insulin secretion decreases, glucagon secretion increases).
• Carb metabolism:
  • Glycogenolysis in the liver releases glucose into the bloodstream.
• Lipid metabolism:
  • Lipolysis in adipose tissue releases free fatty acids and glycerol into the bloodstream.
• Protein metabolism:
  • Protein breakdown increases, supplying amino acids for gluconeogenesis.
• Post-absorptive state processes (catabolic):
  • Glycogenolysis - breakdown of glycogen in the liver.
    • Glucose is released into the blood to maintain normal blood glucose levels.
  • Glycogenolysis in muscle - glycogen breakdown in muscle.
    • Glucose-6-phosphate is used for cellular respiration directly in muscle.
    • Pyruvate or lactate is released into the blood for the liver to convert into glucose if needed.
  • Lipolysis/mobilization/β-oxidation - breakdown of triglycerides in adipose tissue.
    • Free fatty acids and glycerol are released.
    • Fatty acids are transported to tissues for energy.
    • The glycerol is used for gluconeogenesis in the liver.
  • Gluconeogenesis - formation of glucose from noncarbohydrate precursors.
    • Amino acids and glycerol are used as sources.
    • Occurs mainly in the liver to maintain blood glucose levels.
  • Ketogenesis - formation of ketone bodies from fatty acids.
    • Occurs in the liver when glucose levels are low.
    • Ketone bodies can be used as fuel by the brain.
  • Protein breakdown - increasing protein catabolism to provide amino acids for gluconeogenesis and energy production.

Insulin’s Mechanism of Action

• Target cells: liver, muscle cells, and adipose tissue.
• Insulin stimulates the insertion of GLUT-4 transporter proteins into the cell membrane, allowing glucose to enter cells.
• Insulin binding to receptors on target cells stimulates:
  • Glucose uptake.
  • Glycogenesis.
  • Protein synthesis.
  • Lipid synthesis.
• GLUT-4 transporters:
  • Insulin-sensitive glucose transporter proteins.
  • Responsible for glucose uptake in muscle and adipose tissue.
  • Insulin stimulates the translocation of GLUT-4 from intracellular vesicles to the cell membrane.

Insulin Secretion

• Stimulated by:
  • Increased blood glucose levels.
  • Parasympathetic stimulation of the GI tract and pancreas.
  • Amino acids in the bloodstream.
• Amplified by:
  • Gastrointestinal hormones (like gastrin, secretin, GIP).
• Inhibited by:
  • Stress hormones (epinephrine, norepinephrine, cortisol).
  • Reduced blood glucose levels.

Glucagon Secretion

• Stimulated by:
  • Decreased blood glucose levels.
  • Increased levels of amino acids.
• Factors that influence the stimulus for glucagon secretion:
  • Duration of fasting.
  • Dietary intake of protein.
  • Physical activity.
• Abnormally elevated plasma glucose concentration is called hyperglycemia.
• Causes of hyperglycemia:
  • Diabetes mellitus.
  • Excess intake of carbohydrates.
  • Certain medications.

Type 1 Diabetes

• Type 1 diabetes:
  • Autoimmune disease that destroys beta cells in the pancreas.
  • Results in an absolute deficiency of insulin.
• Causes:
  • Genetic predisposition.
  • Environmental triggers.
• Symptoms:
  • Increased thirst and urination.
  • Excessive hunger.
  • Weight loss.
  • Fatigue.
  • Blurred vision.
  • Slow-healing wounds.
  • Increased infections.
• Treatments:
  • Insulin therapy.
  • Blood glucose monitoring.
  • Healthy diet and exercise.

Type 2 Diabetes

• Type 2 diabetes:
  • Characterized by insulin resistance.
  • The pancreas produces insulin, but the body's cells are unable to respond to it properly.
• Causes:
  • Genetic predisposition.
  • Obesity.
  • Lack of physical activity.
  • Aging.
• Complications:
  • Heart disease.
  • Stroke.
  • Kidney disease.
  • Nerve damage.
  • Retinopathy (eye damage).
  • Amputations.
• Treatment:
  • Lifestyle modifications (diet, exercise, weight loss).
  • Oral medications.
  • Insulin therapy (in some cases).

Protein and Nucleic Acids

• Protein - consists of one or more polypeptide chains folded and coiled into a specific shape (conformation).
  • Makes up 50% of a cell's mass.
  • Functions:
    • Enzymatic reactions.
    • Storage of amino acids.
    • Protection against disease.
    • Transport of substances.
• Other protein functions:
  • Hormonal regulation - insulin.
  • Receptors - nerve cells.
  • Movement - cilia, flagella, muscle contraction.
  • Structural support- hair, skin appendages, connective tissue.
• Amino acids - building blocks of proteins.
  • Contain: Carbon, hydrogen, oxygen, nitrogen, and a variable R-group.
  • Buffering capacities: act as buffers to maintain pH stability.
• R-groups - provide unique properties to amino acids.
  • Types:
    • Non-polar: hydrophobic, repel water (glycine, alanine, valine, leucine, isoleucine, methionine, proline, tryptophan).
    • Polar: hydrophilic, attract water (serine, threonine, cysteine, tyrosine, asparagine, glutamine).
    • Electrically charged:
      • Acidic: carboxyl group in their R-group, release H+ (aspartic acid, glutamic acid).
      • Basic: nitrogen in their R-group, accept H+ (lysine, arginine, histidine).
• Hydrophobic interactions (-) - interactions between nonpolar R-groups.
  • Stabilize protein structure by pushing nonpolar R-groups together in the interior of the protein.
• Polypeptides - chains of amino acids connected by peptide bonds.
• Levels of protein structure:
  • Primary: sequence of amino acids.
  • Secondary: folding of the polypeptide chain into alpha-helices or beta-sheets.
  • Tertiary: 3D shape of the polypeptide chain.
  • Quaternary: arrangement of multiple polypeptide chains.