Regulation of Feeding

How do you calculate the amount of protein catabolized in the body based on urine nitrogen content?

1.1 x Mass N2 in urine x 6.25 = Protein metabolism per day.

On average, how much protein is catabolized by the body on a daily basis?

30 to 50 grams of protein per day.

By percentage, how much nitrogen is eliminated via feces and how much via urine?

90% urine, 10% feces.

Why would leptin decrease insulin secretion if both leptin and insulin work to suppress appetite?

Adipocytes have GLUT4, which is how they absorb glucose for fatty acid synthesis. GLUT 4 is insluin dependent, therefore decreasing insulin will decrease the adipocyte's ability to create and store fats.

What cell type releases Leptin, which nuclei of the hypothalmus does it target, and how are Orexigenic and Anorexigenic neurons effected?

Adipose cells release Leptin in proportion to the amount of lipid they contain. High leptin levels will inhibit Orexigenic Neurons and stimulate Anorexigenic Neurons.

Are POMC neurons orexigenic or anorexigenic?

Anorexigenic and function to reduce food intake and increase metabolism and energy expenditure.

Which nuclei acts as the major site of convergence for hormones that influence feeding behavior?

Arcuate Nuclei.

What structure of the brain contains the neurons responsible for the mechanical control of feeding and what processes fall under this category?

Brain stem contains the motor centers needed for mechainical control of feeding. These processes include, salvation, chewing, swallowing and the rest of digestion.

How does CCK effect Orexigenic and Anorexigenic neurons and why does this make sense physiologically?

CCK is released in response to fats and proteins in the duodenum during digestion. CCK will inhbit orexigenic neurons and stimulate anorexigenic neurons resulting in a decreased drive to feed. This feed back loop prevents over eating.

A person with a respiratory quotent of 1 is primarily undergoing metabolism of what type of dietary substance?

Carbohydrates

True or False. Ghrelin directly inhibits anorexigenic neurons in order to magnify the effects of the orexigenic neurons it stimulates.

False. Stimulation of Orexigenic neurons by ghrelin will lead to inhibition of the anorexigenic neuron via cross-talk synapse, not through a ghrelin receptor on the anorexigenic neuron.

A person with a respiratory quotent of 0.7 is primarily undergoing metabolism of what type of dietary substance?

Fats

How would you expect gastrointestinal hormones, released during digestion, to impact appetite and the drive to eat?

GI hormones released during digestion will suppress appetite and drive to feed.

What type of neuron does ghrelin target in the appetite centers of the brain and what cells secrete ghrelin?

Ghrelin is secreted by Epsilon Cells of the pancreas and PD1 cells of the stomach. Ghrelin will stimulate orexigenic neurons in the arcuate nuclei resulting in increased hunger.

Why would high levels of glutamate in the blood increase the desire to eat?

Glutamate is synthesized in order to transport amines, produced by protein catabolism, to the liver or kidney for processing and excretion. High levels of Glutamate indicate that the body is out of glucose and has shifted to amino acid metabolism for fuel. (AA metabolism will continue for a while, then switch to fats, and then back to protein...right before you die)

What structures of the brain are responsible for controlling appetite?

Hypothalmus in conjuction with Amygdala and Pre-Frontal Cortex contain the hunger, feeding, and saiety centers.

When the body is exposed to cold temperatures, what neurotransmitter is released in the hypothalmus and how does this effect the drive to feed?

In cold temperatures, neurons in the hypolamic thermal regulatory center will release GABA, or gamma-aminobutyric acid. Cross talk between neurons means GABA can be seen by appetite centers. GABA increases the drive to eat.

How does leptin effect the secretion of corticotropin releasing hormone and what impacts does this have on appetite?

Increases CRH secretions leading to decreased appetite. CRH is released by the paraventricular nucleus in response to stress.

Does leptin increase or decrease sympathetic nerve activity?

Increases it.

How does Insulin effect Orexigenic and Anorexigenic neurons and why does this make sense physiologically?

Insulin is released during the intestinal phase of digestion in response to GIP and presence of food in the GI tract. Insulin will inhibit the orexigenic neurons and stimulate anorexigenic neurons leading to a decrease in drive to feed. This feedback loop prevents over eating.

What is the function of the lateral nuclei and what does stimulation or inhibition of this center result in?

Lateral Nuclei is the feeding center of the brain. Stimulation results in voracious feeding. Inhibition results in lack of interest in eating.

Name the nuclei in the hypothalmus that deal with hunger and the regulation of food intake.

Lateral Nuclei. Ventromedial Nuclei. Paraventricular Nuclei. Dorsomedial Nuclei. Arcuate Nuclei.

How does Leptin effect Orexigenic and Anorexigenic neurons and why does this make sense physiologically?

Leptin will inhibit Orexigenic and therefore decrease the drive to feed. Anorexigenic neurons will be stimulated which will further decrease the drive to feed. Plasma Leptin levels are proportional to the amount of adipocytes, and therefore stored fat/energy. Abundant energy stores in the body decreases the need to feed.

Is leptin a long term or short term regulatory hormone for appetite and feeding?

Long term as leptin levels are a surrogate for total body energy stores in the form of fat. Long term regulation deals with energy stores, short term deals with preventing over eating.

In the arcuate nuclei, what neurotransmitters do Orexigenic and Anorexigenic neurons release when stimulated?

Orexigenic: Release neuropeptide Y (NpY) and Agouti-Related Protein (AGRP). Anorexigenic: Release alpha-melanocyte stimulating hormone (aMSH) and Cocain & amphetamine related transcript (CART).

What are the physiological consequences of stimulation of Orexigenic and Anorexigenic neurons?

Orexigenic: Will synapse with Paraventricular Nuclei resulting in increased drive to feed and decreased energy expenditure. Anorexigenic: Will synapse with PVN resulting in decreased drive to feed and increased energy expenditure.

A person with a respiratory quotent of 0.8 is primarily undergoing metabolism of what type of dietary substance?

Protein

What is the difference between Respiratory Quotent and Respiratory Exchange Ratio if they are both defined as the ratio of CO2 output to O2 consumption?

RQ is the theoretical CO2 output per molecule of Oxygen given a particular metabolic pathway. RER is the measured CO2 output per molecule of Oxygen over a particular time span. RQ = RER when RER is measured for more than an hour.

Is gastrointestinal distension a long or short term regulator of food intake?

Short term.

In general short tem and long term regulation of food intake are concerned with what with regards to food intake and energy stores?

Short-term regulation mechanisms prevent over eating. Long-term regulation mechanisms ensure the body has adequate energy stores such as fat.

How does stimulation of the Oxregenic neurons effect the paraventricular nuclei and what are the physiological consequences?

Stimulation of oxregenic neurons results in the release of Neuropeptide Y and AGRP. NPY will stimulate PVN and inhibit anoxergenic neurons resulting in increased food intake and decreased energy expenditure.

Through what nerve do gastric distension signals reach the hunger centers of the brain?

Vagus nerve.

What is the function of the Ventromedial nuclei and what does stimulation or inhibition of this center result in?

Ventromedial nuclei is the satiety center of the brain. Stimulation induces the feeling of nutritional satisfaction and a reduction in the drive to eat. Inhibition results in voracious and continuous feeding.