starch

**Structure** - Amylose (~20-30%): unbranched helical chain of glucose linked by α-1,4 glycosidic bonds. - Amylopectin (~70-80%): branched, with α-1,4 linkages in the chains and α-1,6 branch points about every 24-30 residues. - Glycogen is the animal analog. It has the same linkage types but is more highly branched (every ~8-12 residues). - Cellulose is the contrast: β-1,4 linkages, which humans cannot digest.

**Digestion (high-yield)** 1. Mouth: salivary α-amylase (ptyalin) cleaves internal α-1,4 bonds. It is inactivated by gastric acid. 2. Small intestine: pancreatic α-amylase continues digestion. It produces maltose, maltotriose, and α-limit dextrins (which contain the α-1,6 branch points). 3. Brush border enzymes: - Maltase (glucoamylase) cleaves maltose and maltotriose. - Isomaltase (α-dextrinase) cleaves α-1,6 branch points. - Sucrase-isomaltase is a single complex with both activities. 4. Absorption: glucose and galactose enter enterocytes via SGLT-1 (secondary active transport with Na⁺). Fructose enters via GLUT-5. All exit the basolateral side via GLUT-2. - Amylase cannot cleave α-1,6 bonds or terminal α-1,4 bonds. It is an endoglycosidase.

**Clinical correlations** - Acute pancreatitis: elevated serum amylase and lipase (lipase is more specific). - Amylase is also found in saliva (mumps, parotitis), so a rise in amylase is not specific to the pancreas. - Pancreatic insufficiency (chronic pancreatitis, cystic fibrosis): malabsorption with steatorrhea. Fat malabsorption is more prominent because lipase reserve is lower and starch digestion is partly compensated by salivary amylase and brush border enzymes. - Acarbose and miglitol: α-glucosidase inhibitors used in type 2 diabetes. They block brush border digestion of starch and disaccharides, which reduces postprandial hyperglycemia. Adverse effects are flatulence, diarrhea, and abdominal discomfort from bacterial fermentation of undigested carbohydrate. Use with hypoglycemia treated with glucose (not sucrose) because sucrose digestion is blocked. - Congenital sucrase-isomaltase deficiency: osmotic diarrhea and bloating after sucrose or starch ingestion. - Lactase deficiency is the more common disaccharidase deficiency, but it affects lactose, not starch. - Glycogen storage diseases involve defects in glycogen (not dietary starch) metabolism. Examples: von Gierke (G6Pase), Pompe (lysosomal α-1,4-glucosidase), Cori (debranching enzyme), Andersen (branching enzyme), McArdle (muscle glycogen phosphorylase). - Resistant starch escapes small-intestinal digestion and is fermented by colonic bacteria into short-chain fatty acids (butyrate, the main fuel for colonocytes). - Glycemic index: highly processed starches are digested quickly and raise blood glucose more than resistant or high-fiber starches.

**Lab/pathology note** - Iodine stains starch blue-black (amylose forms a helical complex with iodine). This is used in lab tests, and in the historical iodine test for starch. - Starch granules and "starch" artifact: starch from surgical glove powder can contaminate histology specimens and cause granulomatous peritonitis (a historical complication). Under polarized light they show a "Maltese cross" appearance.