Metabolic states

Small intestine

Allows for absorption of nutrients during absorptive state

Oxidation

Provides fuel to cells

Small intestine

Allows for absorption of nutrients during absorptive state

Oxidation

Provides fuel to cells

Glycogenesis

Stores excess glucose in skeletal muscle and hepatocytes

Lipogenesis

Converts glucose into triglycerides stored in adipocytes/ hepatocytes

Protein synthesis

Building block structural materials for cells

Insulin

Released when theirs an increase of blood glucose

Postabsorptive state

Begins once nutrient absorption is complete slows down anabolic processes

Glucogenic amino acid

Is released when breakdown of proteins in muscle cells occurs which then releases into blood

Ketogenesis

Converts fatty acids to ketone bodies and release into blood

Release of glucose

Gluconeogenesis and glycogenolysis in hepatocytes

Lipolysis

In adipocytes releases fatty acids into blood

Cells fuel

Oxidation of molecules

Glucose sparing

cells catabolize newly delivered fatty acids preferentially to conserve glucose for cells of nervous system; non-nervous system cells can also use ketone bodies and amino acids for fuel

Pancreatic hormone glucagon

Released when blood glucose level DROPS; triggers glycogenesis and gluconeogenesis in liver

Epinephrine and norepinephrine

Stimulates lipolysis in adipose tissue and glycogenolysis in skeletal muscle ( can only be used in skeletal muscle)

Cortisol

Stimulates gluconeogenesis and processes that release glucogenic precursor into blood

Fasting

Prolonged period during which little to no food is consumed

Protein wasting

Consequence of fasting, first noticeable in MUSCLE TISSUE, DEGRADATION of muscle proteins results in WEAKNESS and FATIGUE, along with significant DECREASE in muscle mass

Feeding

Controlled by variety of HORMONAL and NEURAL signals; stimulate and or inhibits feeding related nuclei in hypothalamus

Satiety center

Elicits feeling of FULLNESS; INHIBITS desire to eat

Hunger center (feeding center)

Elicits feelings of HUNGER; STIMULATES desire to eat

Long term regulation

Of feeding is primarily HORMONAL

Leptin

Hormone produced by ADIPOCYTES; makes you feel full and INHIBITS neurons in hunger center

Ghrelin

Produced by STOMACH mucosal cells; STIMULATES neurons in hunger center to promote hunger

Drop in leptin levels

Stimulates hunger center allowing hunger center neurons to become activated

Short term signals

Can also inhibit or stimulate feeding

Insulin

Released in response to feeding; DECREASES food intake

Cholecystokinin

Induces satiety feeling full; released because of proteins and fats

Low level of glucose in blood

Known as HYPOGLYCEMIA stimulates hunger center and release of orexin

Promote hunger

Orexins and neuropeptides

Indirectly suppress

Caused when the stomach is stretched; suppress hunger center and decrease release of hunger related neurotransmitters