Question

____ is NOT a role of the liver, a vital organ to the functioning and health of the body.

a. Urea formation

b. Synthesis and/or re-organization of blood proteins

c.Inactivation of hormones and drugs

d.Detoxification of poisons such as alcohol and nicotine

e.Production of hormones which regulate hunger and thirst

Answer 1

Answer is (E) Production of hormones which regulate hunger and thirst.

Justification : Whenever the body is deprived of water,the thirst centre is activated and as a result additional action of Vasopressin(ADH) by the positive feedback mechanism produced by the hypothalamus. Thus ADH retains water from the kidney tubules and causes retention of water content in the body. Also important mechanisms of hunger and thirst are explained below.

THIRST

An appetitive mechanism under hypothalamic control is thirst. Drinking is regulated by plasma osmolality and extracellular  fluid (ECF) volume in much the same fashion as vasopressin secretion. Water intake is increased by increased effective osmotic pressure of the plasma , by decreases in ECF volume, and by psychologic and other factors.

Osmolality acts via osmoreceptors,receptors that sense the osmolality of the body fluids. These osmoreceptors are located in the anterior hypothalamus.Decreases in ECF volume also stimulate thirst by a pathway independent of that mediating thirst in response to increased plasma osmolality .Thus, hemorrhage causes increased drinking even if there is no change in the osmolality of the plasma. The effect of ECF volume depletion on thirst is mediated in part via the renin–angiotensin system . Renin secretion is increased by hypovolemia and results in an increase in circulating angiotensin II. The angiotensin II acts on the subfornical organ, a specialized receptor area in the diencephalon , to stimulate the neural areas concerned with thirst. Some evidence suggests that it acts on the organum vasculosum of the lamina terminalis (OVLT) as well. These areas are highly permeable and are two of the circumventricular organs located outside the blood–brain barrier . However, drugs that block the action of angiotensin II do not completely block the thirst response to hypovolemia, and it appears that the baroreceptors in the heart and blood vessels are also involved. The intake of liquids is increased during eating (prandial drinking).The increase has been called a learned or habit response, but it has not been investigated in detail. One factor is an increase in plasma osmolality that occurs as food is absorbed. Another may be an action of one or more gastrointestinal hormones on the hypothalamus. When the sensation of thirst is obtunded, either by direct damage to the diencephalon or by depressed or altered states of consciousness, patients stop drinking adequate amounts of fluid. Dehydration results if appropriate measures are not instituted to maintain water balance. If the protein intake is high, the products of protein metabolism cause an osmotic diuresis  and the amounts of water required to maintain hydration are large. Most cases of hypernatremia are actually due to simple dehydration in patients with psychoses or hypothalamic disease do not or cannot increase their water intake when their thirst mechanism is stimulated. Lesions of the anterior communicating artery can also obtund thirst because branches of this artery supply the hypothalamic areas concerned with thirst.

Hunger  

The Hypothalamus Contains Hunger and Satiety Centers. Several neuronal centers of the hypothalamus participate in the control of food intake. The lateral nuclei of the hypothalamus serve as a feeding center, and stimulation of this area causes an animal to eat voraciously (hyperphagia). Conversely, destruction of the lateral hypothalamus causes lack of desire for food and progressive inanition, a condition characterized by marked weight loss, muscle weakness, and decreased metabolism. The lateral hypothalamic feeding center operates by exciting the motor drives to search for food. The ventromedial nuclei of the hypothalamus serve as a major satiety center. center. Electrical stimulation of this region can cause complete satiety, and even in the presence of highly appetizing food, the animal refuses to eat (aphagia). Conversely, destruction of the ventromedial nuclei causes voracious and continued eating until the animal becomes extremely obese, sometimes weighing as much as four times normal. The paraventricular, dorsomedial, and arcuate nuclei of the hypothalamus also play a major role in regulating food intake. For example, lesions of the paraventricular nuclei often cause excessive eating, whereas lesions of the dorsomedial nuclei usually depress eating behavior. The arcuate nuclei are the sites in the hypothalamus where multiple hormones released from the gastrointestinal tract and adipose tissue converge to regulate food intake, as well as energy expenditure. Much chemical cross talk occurs among the neurons on the hypothalamus, and together, these centers coordinate the processes that control eating behavior and the perception of satiety. These hypothalamic nuclei also influence the secretion of several hormones that are important in regulating energy balance and metabolism, including those from the thyroid and adrenal glands, as well as the pancreatic islet cells.

  

The hypothalamus receive

(1) neural signals from the
gastrointestinal tract that provide sensory information
about stomach filling;

(2) chemical signals from nutrient in the blood (glucose, amino acids, and fatty acids) that
signify satiety;

(3) signals from gastrointestinal hormones;
(4) signals from hormones released by adipose tissue; and
(5) signals from the cerebral cortex (sight, smell, and
taste) that influence feeding behavior.