Biochemistry II - Exam 4 (chapter 27)

BMI: formula

Weight (kg) / height ² (m)

BMI: weights

• obese: >30

• Overweight: 25-30

• Normal: 18.5-25

• Underweight: <18.5

Caloric homeostasis

• Means of regulating body weight

• The ability to maintain adequate but not excessive energy stores

Pathological conditions associated with being overweight

• type 2 diabetes (insulin resistant)

• Hypertension

• Coronary heart disease (arteries can’t deliver enough O2-enriched blood to heart)

info regarding satiation/hunger feelings: satiation

• signals from GI tract induce feelings of satiety

• Cholecytokin (CCK) is a family of small peptide hormones secreted by cells of the intestine following a meal

• CCK binds to its receptor in nerve cells, which related signals to the brain, causing increased feelings of satiety

• Glucagon-like peptide 1 (GLP-1) is a small peptide hormones secreted secreted by the L cells of the intestine

• Once bound to its receptor, GLP-1 induces feelings of satiety in the brain and potentiates insulin secretion while inhibiting glucagon secretion

• CCK and GLP-1 are just two of many GI peptides that regulate food intake

info regarding satiation/hunger feelings: Appetite

• adipocytes secrete signals called adipokines.

• A key one, leptin, is secreted in direct proportion to the amount of body fat

• When leptin levels fall, hypothalamic neurons increase secretion of neurotransmitters NPY and AgRP, resulting in increased appetite

• When leptin levels rise, NPY and AgRP levels fall, whereas secretion of the neurotransmitters MSG rises, leading to decreased appetite

• Insulin is secreted by pancreatic beta cells when blood-glucose levels are high

• Insulin also appears to act in the brain to decrease levels of NPY and AgRp

info regarding satiation/hunger feelings: Appetite suppressing signals

CCK, GLP-1, GLP-2, amylin, bombesin, enterostatin, apolipoprotein A-IV, gastric inhibitory peptide

info regarding satiation/hunger feelings: Appetite enhancing signals

Ghrelin (secreted in the stomach)

Which protein rich/carbohydrate low diet helps with body weight

• protein consumption, which seems to induce a feeling of satiation more effectively than do fats or carbohydrates

• Proteins require more energy to digest than do fats or carbohydrates, and the increased energy expenditure contributes to weight loss

Why overnutrition and inactivity can lead to insulin insensitivity

• Check out slides 13-15 in Ch. 27

• Overnutrition and inactivity can lead to excess ATP products (which is bad... See slide 15). 

• Also, excess fats can end up storing in tissues other than adipose (which is bad... see slide 13 about metabolic syndrome). 

• Lastly, slide 14 discusses how excess fat can lead to insulin insensitivity.  Inactivity means you have mitochondria overload, etc. (again, slide 13).

Why exercise can beneficially alter the biochemistry of cells

• mitochondrial biogenesis is stimulated by muscular activity

• Exercise is known to help prevent or treat a host of pathological conditions, including metabolic syndrome and type 2 diabetes

• Calcium released during muscle contraction can also act as a secondary messenger to activate signaling pathways that stimulate mitochondrial biogenesis

• Fatty acids, acting through a different signal transduction pathway, increase the fatty acid oxidation capability of mitochondria

• Increased mitochondrial biogenesis and increased fatty acid oxidation prevents insulin insensitivity

Know what goes on during starved-fed cycle: what is it

• Physiological response to a fast

• Blood glucose levels must be maintained during fasting and subsequent eating (3 steps)

Know what goes on during starved-fed cycle: well fed state (1)

• characterized by insulin secretion

• The presence of insulin stimulates glucose uptake and glycogen synthesis In muscle, adipose tissue, and liver while suppressing gluconeogensis in the liver

• Insulin stead stimulates glycolysis in the liver

Know what goes on during starved-fed cycle: early fasting stage (2)

• characterized by a drop in blood glucose levels

• Physiological response is a decrease in insulin secretion and an increase in glucagon secretion

• Glucagon restores blood-glucose levels by stimulating glycogen breakdown and gluconeogenesis in the liver

• Glucagon also stimulates fatty-acid mobilization from adipose tissue, causing a shift in fuel utilization in muscle from glucose to fatty acid

Know what goes on during starved-fed cycle: refed state (3)

• begins with the ingestion of a meal

• Fatty acids are processed normally but liver does not initially absorb glucose, leaving this fuel in the blood for use by other tissues

• Liver remains in the gluconeogenic mode in order to replenish its own glycogen store

• As glucose levels continue to rise, the liver begins to remove it from the blood and use it for fatty acid synthesis

Metabolic adaptions in prolonged starvation minimize protein degradation

• a key metabolic priority during prolonged fasting is to maintain glucose homeostasis

• During initial stages of prolonged fasting, proteins are degraded and the carbon skeleton are used as gluconeogenic precursors

• Another metabolic priority is to preserve protein. This is accomplished by shifting fuel use from glucose to fatty acids

• Fatty acids are mobilized by the adipose tissues for use by peripheral tissues in order to allow continued use of glucose by the brain

• The liver converts fatty acids into ketone bodies, which after several weeks of starvation become the major fuel for the brain