Key words

• Glucose: a hexose monosaccharide that serves as a monomer for multiple disaccharides + polysaccharides

• Glycogen: a branched-chain polymer of glucose monomers that’s often used for the purposes of energy storage in human cells

• Glucagon: an anti-hypoglycemic hormone that gets released in the event of blood glucose levels getting below the healthy range as part of homeostasis

• Glycolysis: the enzyme-initiated breaking-down of glucose into different molecules as the first stage of respiration

• Gluconeogenesis: the liver-based formation of glucose from non-carb sources like amino acids

• Glycogenesis: the synthesis of glycogen that involves adding glucose monomers to glycogen chains for improved energy storage

• Glycogenolysis: the breaking-down of glycogen into its individual glucose monomers

Healthy blood glucose level guide (in mg/dL0

• Before breakfast - 100 w/o diabetes/130 w/ diabetes

• 2 hours after a meal - 140 w/o diabetes/180 w/ diabetes

• At bedtime - 120 w/o diabetes/90-150 w/ diabetes

Potential symptoms of hypo/hyperglycemia

• Hypoglycemia: sweating/fatigue/dizziness/etc. (+ cardiac failure/a coma in extreme cases) due to the mitochondria in bodily cells not having enough glucose to respire for ATP production and many cells losing more energy than they gain as a result

• Hyperglycemia: increased appetite/excessive thirst/vision blurring due to too many glucose molecules diffusing into bodily cells via their plasma membranes and many cells being unable to cope as a result

The pancreas

• Secretes enzymes like amylase and lipase into the bile duct’s bloodstream so can be considered an endocrine gland

• Has a pancreatic duct connecting it with the bile duct that’s made up of islets of Langerhans

• Contains alpha-cells that manufacture + secrete glucagon as well as beta-cells that do this for insulin

The pancreatic negative feedback method

For increasing glucose concentrations

1. Pancreatic alpha- and beta-cells get stimulated by increased blood glucose levels (beta-cells especially produce insulin whereas alpha-cells produce no glucagon at all)

2. Insulin circulates in bloodstream to bind to target cells’ transmembrane insulin-receptor glycoproteins (especially targeting cells in muscle + liver + adipose tissue)

3. Plasma-membrane glycoproteins increase their glucose absorption levels (compare: collecting ducts with higher water levels) - the glucose can only be absorbed via the GLUT4 (muscle) + GLUT1 (brain) + GLUT2 (liver) transporter proteins for glucose

4. Insulin affects hepatocytes in ways like increasing glucose usage in respiration + stimulating glycogenesis (which produces glycogen for short-term storage) + activating glucokinase for phosphorylating glucose to prevent it from leaving cells thru transporter proteins

5. Some glucose that doesn’t get converted into glycogen will be stored as fats in the longer-term

For decreasing glucose concentrations

1. Pancreatic beta-cells stop releasing insulin so glucagon can be produced + secreted from the alpha-cells in the islets of Langerhans (liver/muscle cell glucose uptake decreases as a result)

2. Glucagon then circulates in the bloodstream so it can bind to receptors specific for it on the hepatocytes

3. The binding of glucagon to hepatocyte receptors stimulates hepatocytes to activate glycogen phosphorylase (which is heavily involved in glycogenolysis) + convert amino acids/lipids into intermediate metabolites for gluconeogenesis

4. Glucose then accumulates inside hepatocytes so it can diffuse out into the bloodstream through GLUT2 proteins (thus increasing blood glucose concentrations) - no response occurs in muscle cells due to their lack of glucagon receptors