1 Quiz 07 Results Question 1: Multiple Choice Average Score 0.47059 points Which one of the following stimulates both insulin and glucagon secretion? Correct Percent Answered hyperglycemia 1.176% somatostatin 1.176% cortisol 2.353% hypoglycemia 1.176% a high protein meal 94.118% Question 2: Multiple Choice Average Score 0.42941 points While volunteering with a medical relief mission in Africa, a college student sampled some local food of dubious origin, and came down with a bad case of diarrhea. Unable to eat for 3 days, his metabolism switched to using energy sources other than carbohydrates. Which of the following would you not expect to happen? Correct Percent Answered ketosis 0% lipolysis 0% alkalosis 85.882% glycogenolysis 7.059% gluconeogenesis 3.529% uremia (high levels of urea in blood) 3.529% Question 3: Essay The attached figure (Glucose Tolerance Graph.jpg) shows results of glucose tolerance tests for 3 male patients. Glucose tolerance tests involve measuring plasma [glucose] following oral consumption of a glucose-rich solution. Immediately before drinking the sugar solution, the patients had fasted for several hours. Normal fasting plasma glucose is about 80 mg/dL. One of the patients is normal, one has diabetes type 1, and one has chronic liver disease. Identify which patient (A, B or C) is normal, which as diabetes type 1, and which has chronic liver disease. Briefly explain and justify each of your choices. Given Answers Patient C is normal. Patient A has a chronic liver disease. Patient B has diabetes type 1. Patient B is glucose intolerant because the glucose concentration increases substantially and then maintains a high level of glucose hours following intake of the glucose solution suggesting that the patient has defective insulin function thus there is not effective glucose uptake in the body. Patient A maintains a fairly high glucose concentration following ingestion of the glucose solution. This suggests, that there is some deficiency in the glucose uptake. Since the liver has the largest stores of glycogen in the body, we can assume that the liver has a deficiency in glyocogenesis which contributes to Patient B's high plasma glucose levels hours after ingesting glucose solution. However, since patient A most likely has functioning inuslin, there are other methods for glucose uptake stimulated by insulin such as insulin mediated glucose uptake in adipocytes and resting skeletal muscles. Thus, patient A has slightly lower plasma glucose values compared to Patient B.2 Patient C appears to have normal glycemia. His fasting glucose is around 80 mg/dL, which is the value. In addition, patient C's glucose returns to the normal range after the glucose load, indicating that he is body is able to manage glycemia appropriately. Patient A appears to have type 1 diabetes. His fasting plasma glucose is abnormally high, which is a sign that he may be insulin deficient and therefore cannot keep his resting glucose lower. In addition, administration of glucose causes his glycemia to rise to very high levels, followed by a lack of return to normal glucose levels. His glycemia remains at around 200mg/dL after the glucose load, indicating that his body has decreased insulin functioning, which would normally restore glucose levels back to ~80 mg/dL. By process of elimination, Patient B appears to have chronic liver disease. Patient B's fasting plasma glucose is abnormally low. This may be caused by chronic liver disease impairing the ability to break down glycogen into glucose during times of fasting. Normally in a fasted state, the liver will breakdown glycogen stores in response to low blood glucose to maintain homeostasis.; in the fasted state, the liver will also use protein stores to perform gluconeogenesis. In chronic liver disease, the ability to store glycogen is impaired, and the ability to catalyze glycogenolysis is impaired as well; similarly, the liver's ability to make glucose via gluconeogenesis may be dysfunctional in liver disease. After the glucose is administered, patient B's plasma glucose increases dramatically and stays high. This may be explained again by the liver's inability to safely convert glucose into glycogen (glycogenesis) due to chronic liver disease. Chronic liver disease may also damage hepatocyte sensitivity to insulin or disrupt the signaling cascade present in hepatocytes. Normally, in the fed state, insulin will bind receptors on hepatocytes and trigger a signal cascade leading the the activity of hexokinase. Hexokinase phosphorylates glucose into glucose 6 phosphate, effectively keeping intracellular glucose low, maintaining the glucose concentration gradient. Under normal conditions, this gradient will favor glucose entering the hepatocytes from the plasma, reducing plasma glucose concentrations. In chronic liver disease, this mechanism of keeping plasma glucose low may be disrupted, which explains why patient B retains high glycemia after consuming the glucose load. Patient C is normal. A small rise in [glucose] is followed by a return to normal levels. Patient A has diabetes as they have constantly high levels of glucose. Patient B has liver disease because they have an intially low concentration of glucose. Patient A has diabetes type 1. Looking at the graph, his glucose level in a fasting state is much higher compared to the others. There is also a large and prolonged rise in plasma glucose after the oral consumption of a glucose-rich solution. Both of these markers are due to insufficient insulin secretion. Patient B has chronic liver disease. He demonstrates low glucose levels in a fasting state at the start of the test. Plasma glucose is maintained by using glycogen stores; since his liver is unable to synthesize and store enough glycogen, plasma glucose levels are low. He also shows a large and prolonged rise in plasma glucose. Thus, there is deficient glucose uptake and glycogen synthesis in liver. Patient C is normal. He has normal glucose levels in a fasting state at the start of the test. There is a moderate rise in plasma glucose after consumption of the glucose solution, and a return to normal levels can be seen. Patient C is normal; his blood glucose spikes briefly and returns to normal levels within 2 hours. Patient A has diabetes type 1; his resting blood glucose levels are higher than the other two patients, and he remains hyperglycemic hours after the oral