Chapter 23 — Metabolism and Energy

Hunger is promoted by signals such as ghrelin from the stomach and neuropeptide Y/agouti-related protein pathways in the hypothalamus.

Satiety signals include CCK, GLP-1, PYY, leptin, and hypothalamic pathways that reduce food intake.

Leptin is released by adipose cells and signals the brain about energy stores, generally reducing appetite.

Ghrelin is released mainly by the stomach and stimulates hunger.

A brain region involved in stimulating food intake.

A hypothalamic control region involved in suppressing food intake.

Energy balance compares energy stored, energy intake, and energy output; body energy changes according to intake minus output.

Work and heat.

Transport work, mechanical work, and chemical work.

Energy used to move substances across cell membranes.

Energy used to produce movement, such as muscle contraction.

Energy used to synthesize molecules and support growth, maintenance, and storage.

Age and sex, lean muscle mass, activity level, diet and diet-induced thermogenesis, hormones, and genetics.

The lowest rate of energy expenditure needed to maintain basic body functions under standardized resting conditions.

Energy expenditure measured at rest, commonly after an overnight fast.

Short-term energy is stored as ATP; longer-term energy is stored mainly as glycogen and fat.

Primarily in the liver and skeletal muscles.

Approximately 4 kilocalories.

Approximately 4 kilocalories.

Approximately 9 kilocalories.

Fat is compact and contains more than twice the energy per gram as carbohydrate or protein.

A method of estimating metabolic rate using oxygen consumption and carbon dioxide production.

The respiratory exchange ratio, calculated as carbon dioxide production divided by oxygen consumption.

RER = CO₂ produced ÷ O₂ consumed.

It estimates which fuel is being used; values near 0.7 suggest mostly fat oxidation, near 1.0 suggest mostly carbohydrate oxidation, and intermediate values indicate a mixture.

Anabolism builds larger molecules from smaller ones; catabolism breaks larger molecules into smaller ones.

The absorptive state after eating, when nutrients are available and insulin generally dominates.

The postabsorptive state between meals, when stored fuels are mobilized and glucagon generally dominates.

They can be used to produce energy, used for synthesis and growth, or stored as glycogen or fat.

Readily available pools of nutrients in the blood and tissues that can be used or stored.

The glucose pool, free fatty acid pool, and amino acid pool.

By balancing glucose use, glycogenesis, glycogenolysis, gluconeogenesis, and conversion of excess glucose into fat.

By balancing lipolysis, which releases fatty acids, and lipogenesis, which stores them as triglycerides.

By balancing dietary amino acid input, protein synthesis, protein breakdown, and amino acid catabolism.

Excess carbohydrate can be converted into fatty acids and stored as triglycerides.

Excess amino acids cannot be stored as protein directly; they can be deaminated and used for energy or converted into fat.

The body increases gluconeogenesis from lactate, glycerol, and amino acids to maintain blood glucose.

Opposing enzymes are regulated so synthesis and breakdown do not occur at high rates simultaneously; insulin favors storage, while glucagon favors breakdown and glucose release.

Lactate is a useful metabolic intermediate that can be converted back to pyruvate and used for energy or gluconeogenesis.

Acetyl-CoA is a major entry point into the citric acid cycle; other breakdown products can also enter as pyruvate or citric acid cycle intermediates.

Glycolysis, pyruvate oxidation, the citric acid cycle, and oxidative phosphorylation.

Triglycerides are broken into glycerol and fatty acids; glycerol enters glycolysis, while fatty acids undergo beta-oxidation to form acetyl-CoA for the citric acid cycle and oxidative phosphorylation.

Proteins are broken into amino acids, which are deaminated; their carbon skeletons enter glycolysis or the citric acid cycle.

Glucose is oxidized for ATP, stored as glycogen, or converted into fat when present in excess.

Fatty acids and glycerol are assembled into triglycerides and stored; cholesterol and other lipids are also synthesized.

Amino acids are used for protein synthesis; excess amino acids can be deaminated and used for energy or converted into fat.

Glycogenolysis and gluconeogenesis maintain blood glucose.

Lipolysis releases fatty acids and glycerol; fatty acids undergo beta-oxidation and the liver may produce ketone bodies.

Proteolysis releases amino acids, which can be deaminated and used for energy or gluconeogenesis.

Dietary fats are digested; intestinal cells assemble lipids into chylomicrons; chylomicrons enter lymph and then blood; lipoprotein lipase releases fatty acids and glycerol; adipose cells reassemble triglycerides for storage; remnants return to the liver for processing; LDL carries cholesterol to body cells.

Lipoproteins that transport dietary triglycerides and cholesterol from the intestine through lymph into the blood.

It breaks triglycerides in circulating lipoproteins into free fatty acids and glycerol.

Low-density lipoprotein, which carries cholesterol from the liver to body cells.

High-density lipoprotein, which helps transport cholesterol away from tissues and plasma toward the liver.

LDL delivers cholesterol to cells; HDL helps return cholesterol to the liver for processing and removal.

Glycolysis provides glycerol; pyruvate is converted to acetyl-CoA; acetyl units are used to synthesize fatty acids, and one glycerol combines with three fatty acids to form a triglyceride.

Glucose and ketone bodies.

Removal of the amino group from an amino acid, producing ammonia and an organic acid carbon skeleton.

It allows amino acid carbon skeletons to enter energy pathways, but it produces ammonia that must be detoxified.

The liver converts toxic ammonia into urea, which is transported in blood to the kidneys and excreted in urine.

Liver glycogen is broken down; adipose triglycerides release fatty acids and glycerol; muscle uses fatty acids and may release amino acids and lactate; the liver produces glucose and ketones to supply the brain and other tissues.

Breakdown of glycogen to release glucose units.

Synthesis of glucose from non-carbohydrate precursors such as lactate, glycerol, and amino acids.

Lactate, glycerol, and amino acids are converted into metabolic intermediates; these are used to form pyruvate or citric acid cycle intermediates; pathways produce glucose-6-phosphate; and glucose is released by the liver or kidneys.

Breakdown of triglycerides into glycerol and fatty acids.

Lipases split triglycerides into glycerol and fatty acids; glycerol enters glycolysis; fatty acids undergo beta-oxidation; and the resulting acetyl-CoA enters the citric acid cycle or contributes to ketone production.

The process that breaks fatty acids into two-carbon acetyl-CoA units in the mitochondria.

Beta cells of the pancreatic islets.

Alpha cells of the pancreatic islets.

Insulin.

Glucagon.

Increased blood glucose, increased amino acids, gastrointestinal hormones after a meal, and parasympathetic stimulation.

Low blood glucose inhibits insulin secretion.

Increased glucose uptake and oxidation, increased glycogen synthesis, increased fat synthesis, and increased protein synthesis.

They move to the cell membrane in response to insulin and allow glucose uptake, especially in skeletal muscle and adipose tissue.

Muscle contraction stimulates GLUT4 movement to the membrane through pathways that do not require insulin, increasing glucose uptake.

They provide high-capacity glucose transport in tissues such as the liver and pancreatic beta cells and help these cells sense blood glucose.

It stimulates liver glycogenolysis and gluconeogenesis, increasing glucose release into the blood.

Type 1 involves autoimmune destruction of pancreatic beta cells and severe insulin deficiency; Type 2 involves insulin resistance with progressive impairment of insulin secretion.

Insufficient insulin causes hyperglycemia, glucose loss in urine, osmotic diuresis, dehydration, electrolyte loss, increased fat breakdown and ketone production, and potentially diabetic ketoacidosis and coma.

Excess blood glucose enters the filtrate and exceeds reabsorptive capacity, causing glucosuria and osmotic diuresis.

Water loss through osmotic diuresis causes dehydration and stimulates thirst.

Low insulin and high glucagon promote lipolysis and ketone production; excess ketones lower blood pH.

Increase insulin secretion; improve insulin sensitivity; reduce hepatic glucose production; slow carbohydrate digestion or absorption; increase urinary glucose excretion; and mimic or enhance incretin signaling.

A cluster of metabolic risk factors that increases the risk of cardiovascular disease and Type 2 diabetes.

Increased waist circumference, elevated triglycerides, reduced HDL cholesterol, elevated blood pressure, and elevated fasting blood glucose.

Synthesis of glycogen from glucose.

Synthesis of fatty acids or triglycerides for fat storage.

Breakdown of glycogen to provide glucose or glucose-6-phosphate.

Production of glucose from non-carbohydrate precursors.

A three-carbon molecule produced by glycolysis that can be converted to acetyl-CoA or lactate.

A signaling molecule released by adipose tissue that influences appetite, metabolism, and energy balance.

An adipokine released by fat cells that signals energy stores to the brain and generally suppresses appetite.

A pancreatic hormone that promotes glucose uptake and storage and favors anabolic metabolism.

A pancreatic hormone that promotes liver glycogen breakdown and gluconeogenesis to maintain blood glucose during fasting.