Digestion of Carbohydrates
Overview: Carbohydrates are digested and absorbed to provide fuel. Digestion involves mouth, stomach, and small intestine with specific enzymes at each stage. Brush-border enzymes complete final breakdown before absorption.
Key pathways to absorption and fate:
Monosaccharides (glucose, galactose, fructose) cross the brush border in the intestinal lumen and enter the hepatic portal circulation to the liver (mostly, via the hepatic portal vein). They do not primarily enter the lymphatic system as some fats do.
In contrast to fats, absorbed carbohydrates are delivered to the liver for storage or distribution via the portal system.
Why this matters: Understanding where digestion happens helps explain why certain foods affect blood glucose differently and how disorders like lactose intolerance influence nutrient absorption and calcium intake.
Mouth: initial carbohydrate digestion
Salivary glands produce salivary amylase (ptyalin).
Limited carbohydrate digestion occurs in the mouth due to this enzyme.
Bolus formation begins the journey toward the stomach.
Stomach: inactivation of salivary amylase
Food enters stomach; hydrochloric acid (HCl) is secreted.
HCl inactivates salivary amylase; carbohydrate digestion slows/stops in stomach.
Chewing and gastric churning mix food with acid, preparing it for intestinal digestion.
Small intestine: major digestion and absorption
Pancreas secretes pancreatic amylase into the small intestine.
Pancreatic amylase breaks down complex carbohydrates into simpler sugars (disaccharides, oligosaccharides, and monosaccharides as digestion continues).
Brush-border enzymes on enterocytes complete digestion:
Maltose → glucose + glucose via maltase
Sucrose → glucose + fructose via sucrase
Lactose → glucose + galactose via lactase
Some carbohydrate-rich foods contain fiber; indigestible fibers are not digested here and are fermented later in the large intestine.
Fiber and indigestible carbohydrates
Indigestible carbohydrates are also called resistant starches or dietary fiber.
They pass through the small intestine largely intact and are fermented by gut bacteria in the large intestine.
Byproducts include short-chain fatty acids (SCFAs) and gas.
Benefits: add bulk, support gut motility, and slow nutrient absorption, which broadens the opportunity for nutrient extraction and can blunt post-meal glycemic spikes.
Sources of indigestible carbs include seeds, wheat germ, whole grains, amylose (cornstarch), legumes (lentils, peas, beans), unripe bananas, and whole cooked pasta, rice, and potatoes.
Fiber digestion and gas production
Gas production is a normal byproduct of fiber fermentation in some individuals, especially when fiber intake is increased rapidly.
As the gut becomes accustomed to higher fiber, gas production tends to decrease.
Adaptive digestion and-brush border specificity
Brush-border enzymes are tailored to the specific carbohydrate consumed (e.g., maltase for maltose, lactase for lactose, sucrase for sucrose).
Some individuals with lactose intolerance have insufficient lactase activity, leading to undigested lactose reaching the large intestine, causing bloating, gas, cramps, and potentially diarrhea.
Lactose intolerance prevalence varies by population (higher in some Asian, African, and Mediterranean populations) due to genetic and evolutionary factors.
Lactose intolerance does not eliminate the need for calcium; alternative calcium sources (calcium-fortified foods, non-dairy sources like fortified orange juice, tofu with soft bones, canned fish with soft bones, broccoli, aged cheeses, etc.) and calcium supplements can help maintain bone health.
Calcium considerations for lactose intolerance
Calcium is a critical nutrient for bone development and maintenance.
Alternative and fortified sources help meet calcium needs when dairy is limited.
Supplements can be used but should be considered in context with overall diet.
Indigestible Carbohydrates: Functional roles and practical implications
Indigestible carbs (fiber) increase stool bulk and water content, supporting transit time and bowel health.
They stimulate GI motility (peristalsis) and slow down nutrient absorption, which can improve glycemic control and satiety.
Practical foods rich in indigestible carbs: seeds, whole grains, legumes, unripe bananas, whole cooked pasta, rice, potatoes.
Glycemic response and meal composition
Glycemic response: the rate, magnitude, and duration of rise in blood glucose after a food or beverage.
Key factors influencing glycemic response:
Amount of carbohydrate consumed
Type of carbohydrate (refined vs unrefined; simple vs complex)
Other macronutrients in the meal (fat, protein) which slow digestion/absorption
Gastric emptying rate and overall digestion/absorption rate
Visual example of glycemic response with meals:
Fiber-rich meals produce a moderated rise and a steadier glucose level over time (blue line).
Low-fiber meals produce a sharp, higher peak followed by a sharper decline (red line).
Refined vs unrefined carbs:
White bread (refined) vs kidney beans (unrefined): refined carbs tend to spike glucose quickly; unrefined carbs tend to produce a higher-lower peak due to fiber, protein, and fat content slowing digestion.
Mixed meals with fat and protein blunt glucose spikes and prolong satiety, reducing the likelihood of a rapid crash.
Glycemic index concept (brief): a ranking of foods by their glucose response relative to a reference food (glucose or white bread). Foods with high GI cause larger rapid increases in blood glucose than low GI foods.
Example range: simple glucose reference yields high peaks; soybeans (protein + fiber) yield slower, smaller increases.
Class exercise example: peanut butter sandwich vs a slice of white bread
Peanut butter is high in fat and protein, which slows digestion and reduces the peak and speed of glucose rise compared to white bread alone.
Mixed meals typically lead to more moderate postprandial glucose excursions and improved satiety.
Blood glucose regulation and metabolism
Homeostasis: the body maintains blood glucose at a relatively constant level to support cellular function.
Key hormones:
Insulin: released by the pancreas after carbohydrate ingestion; promotes glucose uptake by muscles and adipose tissue and promotes glycogen synthesis in the liver; helps maintain homeostasis after a meal.
Glucagon: released during fasting or low blood glucose; stimulates glycogenolysis in the liver, glycogen breakdown to raise blood glucose; stimulates gluconeogenesis (making glucose from non-carbohydrate sources).
Post-meal (feasting) state:
Blood glucose rises after carbohydrate ingestion.
Insulin is released to reduce blood glucose by promoting uptake and storage (glycogenesis) and utilization of glucose for energy.
Glucose can be used by muscles for energy, stored as glycogen in liver and muscle, or stored as fat in adipose tissue.
Between meals (fasting) state:
Blood glucose falls; glucagon is released to raise glucose by glycogenolysis and gluconeogenesis.
Key brain glucose requirement:
The brain requires about 130\,\text{g/day} of glucose for basic function.
Glucose metabolism: cellular respiration (how carbohydrates make ATP)
Goal: convert glucose to ATP to power cellular processes.
General equation (for context):
C6H{12}O6 + 6\,O2 \rightarrow 6\,CO2 + 6\,H2O + \text{ATP}Four major steps (in mitochondria; aerobic metabolism except for glycolysis):
1) Glycolysis (cytoplasm; anaerobic): one glucose → two pyruvate, produces net gain of 2\,\text{ATP} and gives electrons to the electron transport chain.
2) Acetyl-CoA formation (out of mitochondria; requires oxygen; coenzyme A involvement): 2 pyruvate → 2 acetyl-CoA molecules; yields NADH and prepares for the TCA cycle.
3) Citric acid cycle (Krebs or TCA cycle) (mitochondria; aerobic): acetyl-CoA + oxaloacetate → citrate; yields ATP indirectly via NADH/FADH2; releases CO2 as a byproduct.
4) Electron transport chain (ETC) (mitochondria; aerobic): electrons from NADH and FADH2 drive proton pumping and ATP synthesis via ATP synthase; produces a large amount of ATP and water as a byproduct.Important notes:
Glycolysis occurs in the cytoplasm and does not require oxygen (anaerobic).
Acetyl-CoA formation, TCA cycle, and ETC require oxygen (aerobic).
The energy yield (ATP) is maximized in the ETC, with NADH/FADH2 feeding the chain.
Gluconeogenesis and ketogenesis (fuel during carbohydrate scarcity):
When carbohydrate intake is very low, gluconeogenesis occurs mainly in the liver (and kidneys) to generate glucose from noncarbohydrate substrates (e.g., amino acids).
Ketone bodies can be produced from fatty acids to provide energy, especially for brain, heart, and muscles when carbohydrate is scarce.
Ketosis can occur in states of prolonged low carbohydrate intake or starvation; ketone bodies can accumulate in urine or blood and lower blood pH if excessive (ketoacidosis is a dangerous condition typically associated with poorly managed diabetes).
Ketones and dietary ketosis:
Ketone bodies are an alternative energy source; they are acidic when in excess and can be dangerous if not regulated.
The ketogenic diet promotes ketone utilization by limiting carbohydrate intake; this is typically not sustainable long-term for most people and is not universally healthier than balanced dietary approaches.
Ketosis vs ketoacidosis: ketosis is a controlled metabolic state; ketoacidosis is a dangerous, uncontrolled, rapidly progressing medical emergency characterized by severe hyperglycemia, dehydration, acidosis, and can lead to coma or death if untreated.
Diabetes and health implications of carbohydrate regulation
Types of diabetes:
Type 1 diabetes: autoimmune destruction of insulin-producing beta cells; insulin deficiency; often diagnosed in youth but can occur at any age.
Type 2 diabetes: insulin resistance with eventual decreased insulin production; strongly associated with obesity and sedentary lifestyle; higher prevalence in certain populations.
Gestational diabetes: glucose intolerance during pregnancy; hormonal changes increase risk for mother and baby; can predict later risk of type 2 diabetes for the mother.
Population impact and risk factors:
About 10.5\% of the US population has diabetes (mostly type 2).
Prediabetes: a state where blood glucose levels are elevated above normal but not yet meeting criteria for diabetes; allows for early intervention.
Risk factors include family history, overweight/obesity, sedentary lifestyle, and certain racial/ethnic groups (Native American/Alaska Native, African American, Hispanic).
The obesity-diabetes relationship is strong; many societies experience rising obesity and diabetes as twin epidemics.
Diabetes pathophysiology and clinical presentation:
Classic symptoms: polydipsia (thirst), polyuria (frequent urination), blurred vision, unexplained weight loss.
Untreated or poorly managed diabetes can lead to chronic complications: cardiovascular disease, stroke, kidney failure, blindness, neuropathy, infections, and possible amputations.
Diabetic ketoacidosis (DKA) is a serious complication of uncontrolled diabetes and requires urgent medical care.
Blood glucose patterns in diabetes:
Fasting glucose and postprandial glucose trajectories are altered in diabetes; fasting glucose may be elevated, and postprandial peaks can be higher and more prolonged.
Management aims to keep blood glucose within target ranges to prevent acute symptoms and long-term complications.
Management strategies:
Diet: focus on refined vs unrefined carbohydrates; emphasize dietary fiber, complex carbohydrates, and overall balanced meals to moderate glycemic response.
Exercise: improves insulin sensitivity and helps glucose uptake by muscles.
Medications: Type 1 requires insulin therapy; type 2 may require medications or can be managed with diet and exercise initially; treatment plans are individualized.
The role of dietary guidance and support from healthcare professionals to sustain lifelong management.
Exam information and study resources (session-specific)
Exam feedback and scoring:
Average score around 80/100; maximum observed 96/100.
Some items were adjusted post-exam (two points added for a specific item) to reflect test quality and coverage.
Review procedures for exams:
To review an exam in person, email the teaching assistant (Evelyn) using the address on the syllabus and request an in-person meeting.
In-person reviews allow bringing notes and asking questions; if a question is better addressed by the instructor, they will direct you accordingly.
You have up to two weeks to schedule and attend review meetings.
You may request a grade change or reconsideration if needed, but changes may affect other items as well.
It is not allowed to take exams home or take pictures of exams or screens during review.
Study resources and strategies:
Use the Academic Achievement Center to learn study and note-taking strategies; mattching resources provided by campus and your student fees can help you prepare more efficiently for subsequent exams.
Understand the shift from memorization to processes and regulation in later exams; focusing on understanding mechanisms (glycolysis, gluconeogenesis, regulation of insulin/glucagon) is crucial.
Quick references and key definitions
Glycemic response: rate, magnitude, and duration of rise in blood glucose after a meal.
Homeostasis: maintaining stable internal conditions (e.g., blood glucose) despite external changes.
Glycemic index (GI): a ranking of foods based on their blood glucose response relative to a reference food.
Glycogen: stored form of glucose, primarily in liver and muscles.
Glycogenolysis: breakdown of glycogen to release glucose.
Gluconeogenesis: production of glucose from non-carbohydrate substrates (e.g., amino acids, glycerol).
Ketogenesis: production of ketone bodies (used as alternative energy for some tissues when carbohydrate is scarce).
Insulin: hormone that lowers blood glucose by promoting glucose uptake and storage.
Glucagon: hormone that raises blood glucose by promoting glycogenolysis and gluconeogenesis.
Ketone bodies: acetoacetate, beta-hydroxybutyrate, and acetone produced during fatty acid breakdown; can be used by the brain and other tissues when glucose is scarce.
Lactose intolerance: reduced lactase activity leading to poor digestion of lactose and GI symptoms; calcium considerations become important for bone health.
Diabetes mellitus: chronic condition characterized by dysregulated blood glucose due to insulin deficiency (type 1) or insulin resistance (type 2), with gestational diabetes occurring during pregnancy.
Key numerical references:
Brain carbohydrate requirement: 130\,\text{g/day}
General carbohydrate contribution to calories (dietary guidelines): 45\%\text{ to }65\% of daily calories from carbohydrates
Fasting blood glucose threshold (normal): <100\,\text{mg/dL}
Postprandial blood glucose threshold (normal, ~2 hours after eating): <140\,\text{mg/dL}
Diabetes prevalence in US: \approx 10.5\%
Important enzymes and steps to memorize:
Salivary amylase (mouth)
Pancreatic amylase (small intestine)
Maltase (maltose), Sucrase (sucrose), Lactase (lactose) – brush-border enzymes
Pyruvate → acetyl-CoA (via pyruvate dehydrogenase) in mitochondria
Citric acid cycle (Krebs) and Electron Transport Chain (ETC) in mitochondria
Practical implications for day-to-day life:
Mixing carbohydrates with fats and proteins moderates post-meal glucose response and improves satiety.
Regular fiber intake supports gut health, improves transit time, and moderates nutrient absorption.
Lactose intolerance and calcium intake require attention to non-dairy calcium sources or fortified foods.
Ketosis should be monitored; prolonged ketosis without medical supervision can be dangerous; ketoacidosis is a medical emergency.
Ethical and practical considerations:
Socioecological factors influence diet, access to healthy foods, and diabetes risk (food deserts, cultural dietary patterns, healthcare access).
Culturally tailored nutrition education and prevention strategies are important in reducing disparities in diabetes prevalence and outcomes.
Balanced dietary patterns with emphasis on fiber, whole grains, and physical activity align with general health guidelines and reduce chronic disease risk.