Carbohydrate Metabolism and Hormonal Regulation (Key Points)

Carbs release energy by breaking bonds within ring and branched structures; ATP is produced when bonds are cleaved.
Glucose is the simplest form of carbohydrate energy; dietary carbs and stored forms supply glucose.
Starch types: simple starches like amylose (easily broken down) and more branched amylopectin; amylase breaks starches.
Amylase (α-amylase) acts on starches; present in both pancreas and saliva (amylase s in saliva, amylase p in pancreas).
Monosaccharides from digestion: basic units like glucose, fructose, galactose; monosaccharides typically have $4\leq n\leq 8$ carbons; many are reducing sugars (contain an aldehyde group).
Monosaccharides (3 main): glucose, fructose, galactose; sources: glucose (general), fructose from fruit, galactose from dairy.
Disaccharides: maltose (glucose + glucose), lactose (glucose + galactose), sucrose (glucose + fructose).
Polysaccharides: many monosaccharide units; starch, amylose, amylopectin; glycogen as storage form in liver and muscles; dietary fiber is more complex polysaccharide.
Digestion progression: polysaccharides → disaccharides → monosaccharides → absorption into blood; absorbed glucose goes to liver first.
Liver and storage: excess glucose stored as glycogen (glycogenesis) in liver and muscles; excess can be converted to fat (adipose tissue).
Carbohydrates and energy: simple carbs release energy quickly; complex polysaccharides release glucose more steadily.

Glucose formula: $ext{C}<em>6 ext{H}</em>{12} ext{O}_6$
Monosaccharides: basic unit with a carbon backbone and oxygen-containing groups; some are reducing sugars due to aldehyde/ketone groups.

Amylase main enzyme for starch breakdown; amylase s (salivary) initiates breakdown in the mouth; amylase p (pancreatic) continues in the small intestine.
Disaccharides also require specific enzymes (e.g., lactase for lactose) to release glucose.
Absorption: monosaccharides cross gut into blood; liver stores glucose as glycogen; excess stored as fat in adipose tissue.

Glycolysis: glucose → pyruvate (produces ATP); under anaerobic conditions, pyruvate → lactate; under aerobic conditions, pyruvate enters the Krebs cycle.
Key states: fed (post-meal) vs fasting (between meals).
Gluconeogenesis: formation of glucose from non-carbohydrate sources (e.g., amino acids, lipids).
Glycogenolysis: breakdown of glycogen to glucose; glycogenesis: formation of glycogen from glucose.
Glycogen (storage form of glucose) location: liver and muscle; muscles store for own use; liver maintains blood glucose.
Hormonal control: insulin lowers blood glucose; glucagon raises blood glucose.

Insulin: produced by beta cells in the islets of Langerhans; decreases blood glucose; promotes cellular uptake of glucose; stimulates glycogenesis and lipogenesis.
Glucagon: produced by alpha cells; increases blood glucose; stimulates glycogenolysis and gluconeogenesis.
Other hormones increasing glucose: epinephrine (adrenaline), growth hormone/ACTH (pituitary), glucocorticoids (cortisol), thyroid hormones (increase glycogenolysis).
Which is not like the others? Insulin decreases blood glucose; all others tend to increase it.

Fed state: high glucose after a meal; insulin rises; glycolysis and glycogenesis promoted; blood glucose drops as glucose moves into cells and is stored.
Fasting state: no immediate glucose intake; glucagon rises; glycogenolysis and gluconeogenesis raise blood glucose; glycogen stores used first, then amino acids/lipids for glucose synthesis.
Hormonal control: insulin (fed) vs glucagon (fasting); these regulate blood glucose and storage vs release.
Concept: these pathways form a continuous loop driven by nutritional state.

Hyperglycemia: blood glucose > $126\ \,\mathrm{mg/dL}$ ; common in diabetes mellitus (types 1 & 2, gestational).
Hypoglycemia: blood glucose < $30\ \,\mathrm{mg/dL}$ (dangerous; brain is highly sensitive to low glucose); can result from glucagon/insulin imbalances, tumors (insulinomas), drugs, or mismanaged diabetes.
Diabetes overview: Type 1 requires exogenous insulin; lack of insulin leads to high blood glucose; other hormones normally help raise glucose if insulin is deficient, but not always enough.
Lactic acidosis risk: under hypoxic conditions or liver dysfunction, excess lactate leads to acidosis; important in diabetics with shock, sepsis, or heavy exercise.

Glycogen storage disease: inherited deficiency in one of eight enzymes that break down glycogen; causes hepatomegaly, growth issues, hypoglycemia, and potential CNS problems.
Effects: impaired glycogen breakdown in liver reduces available glucose; liver and muscle glycogen storage are affected; can lead to fatigue and cramps due to glycogen buildup and energy shortage.

Insulin = fed state, decreases glucose, promotes glycogenesis and lipogenesis.
Glucagon = fasting state, increases glucose, promotes glycogenolysis and gluconeogenesis.
Epinephrine, cortisol, growth hormone, thyroid hormones = generally raise blood glucose or promote glucose production.
Lactic acidosis risks increase with poor oxygen supply or liver dysfunction; monitor in diabetics.
Glycogen storage disease = enzyme deficiency leading to glycogen buildup in liver/muscle and hypoglycemia.