Question

1. An individual has low blood oxygen levels, due to insufficient numbers of circulating red blood cells. (The erythrocytes are completely healthy; there’s just not enough of them.) Describe the processes by which the body stimulates the production of new erythrocytes. Your response should include a review of all body cells and structures capable of detecting low oxygen levels, the body responses that stimulate erythrocyte production, and the actual synthesis and maturation process in the red bone marrow. In addition, any short-term body processes that compensate for the low blood oxygen levels not involving erythrocyte production should be discussed in detail as well.

2. An individual has low blood glucose levels—not low enough to cause symptoms, but enough to cause the body to attempt a restoration to normal levels. Describe all processes by which the body induces the increase of blood sugar levels. Your response should include a review of all body cells and structures capable of detecting low glucose levels, the body responses that stimulate glucose production, and all processes for the actual synthesis of glucose. (While this is not a biochemistry class, a thorough discussion of the two major glucose production pathways is expected; a couple sentences for each will not suffice for full credit.)

Answer 1

-Body's short term effect to deal with low oxygen levels is

The Bohr effect describes how the affinity of hemoglobin for oxygen changes depending on the local biochemical conditions. An increase in acidity, temperature and the concentration of intermediate chemicals in the conversion of sugar to energy—specifically 2,3-diphosphoglycerate—decreases hemoglobin's affinity for oxygen, causing oxygen to diffuse into the tissues.

Low oxygen levels CAUSES OXYGEN-HAEMOGLOBIN DISSOCIATION CURVE TO SHIFT RIGHT DUE TO DECREASED AFFINITY OF HAEMOGLOBIN TO OXYGEN. THIS DECREASED AFFINITY TO OXYGEN PROMPTS RELEASE OF OXYGEN FROM HAEMOGLOBIN TO TISSUES MORE EFFICIENTLY.

-review of all body cells and structures capable of detecting low oxygen levels

The respiratory center is composed of several groups of neurons located bilaterally in the medulla oblongata and pons of the brain stem, as shown in Figure 41-1. It is divided into three major collections of neurons: (1) a dorsal respiratory group, located in the dorsal portion of the medulla, which mainly causes inspiration; (2) a ventral respiratory group, located in the ventrolateral part of the medulla, which mainly causes expiration; and (3) the pneumotaxic center, located dorsally in the superior portion of the pons, which mainly controls rate and depth of breathing.

It is believed that none of these is affected directly by changes in blood carbon dioxide concentration or hydrogen ion concentration. Instead, an additional neuronal area, a chemosensitive area, is located bilaterally, lying only 0.2 millimeter beneath the ventral surface of the medulla. This area is highly sensitive to changes in either blood Pco2 or hydrogen ion concentration, and it in turn excites the other portions of the respiratory center. Oxygen, in contrast, does not have a significant direct effect on the respiratory center of the brain in controlling respiration. Instead, it acts almost entirely on peripheral chemoreceptors located in the carotid and aortic bodies, and these in turn transmit appropriate nervous signals to the respiratory center for control of respiration.

- erythrocytes production of body due to anemia

Erythropoietin Stimulates Red Cell Production, and Its Formation Increases in Response to Hypoxia. The principal stimulus for red blood cell production in low oxygen states is a circulating hormone called erythropoietin, a glycoprotein with a molecular weight of about 34,000. In the absence of erythropoietin, hypoxia has little or no effect to stimulate red blood cell production. But when the erythropoietin system is functional, hypoxia causes a marked increase in erythropoietin production and the erythropoietin in turn enhances red blood cell production until the hypoxia is relieved. Renal tissue hypoxia leads to increased tissue levels of hypoxia-inducible factor-1 (HIF-1), which serves as a transcription factor for a large number of hypoxia-inducible genes, including the erythropoietin gene. HIF-1 binds to a hypoxia response element residing in the erythropoietin gene, inducing transcription of mRNA and, ultimately, increased erythropoietin synthesis. At times, hypoxia in other parts of the body, but not in the kidneys, stimulates kidney erythropoietin secretion, which suggests that there might be some nonrenal sensor that sends an additional signal to the kidneys to produce this hormone. In particular, both norepinephrine and epinephrine and several of the prostaglandins stimulate erythropoietin production.

-RBC production steps

Blood glucose regulation regulation

1. The liver functions as an important blood glucose buffer system. That is, when the blood glucose rises to a high concentration after a meal and the rate of insulin secretion also increases, as much as two thirds of the glucose absorbed from the gut is almost immediately stored in the liver in the form of glycogen. Then, dur ing the succeeding hours, when both the blood glucose concentration and the rate of insulin secretion fall, the liver releases the glucose back into the blood. In this way, the liver decreases the fluctuations in blood glu cose concentration to about one third of what they would otherwise be. In fact, in patients with severe liver disease, it becomes almost impossible to maintain a narrow range of blood glucose concentration.

2. Both insulin and glucagon function as important feedback control systems for maintaining a normal blood glucose concentration. When the glucose con centration rises too high, increased insulin secretion causes the blood glucose concentration to decrease toward normal. Conversely, a decrease in blood glu cose stimulates glucagon secretion; the glucagon then functions in the opposite direction to increase the glu cose toward normal. Under most normal conditions, the insulin feedback mechanism is much more impor tant than the glucagon mechanism, but in instances of starvation or excessive utilization of glucose during exercise and other stressful situations, the glucagon mechanism also becomes valuable.

3. Also, in severe hypoglycemia, a direct effect of low blood glucose on the hypothalamus stimulates the sym pathetic nervous system. The epinephrine secreted by the adrenal glands further increases release of glucose from the liver. This also helps protect against severe hypoglycemia.

4. And finally, over a period of hours and days, both growth hormone and cortisol are secreted in response to prolonged hypoglycemia. They both decrease the rate of glucose utilization by most cells of the body, converting instead to greater amounts of fat utilization. This, too, helps return the blood glucose concentration toward normal.

-PATHWAYS OF GLUCONEOGENESIS