3 60Patients taking metformin are at increased risk of developing lactic acidosis. How doesmetformin act to increase this risk?Metformin stimulates the consumption of pyruvate via gluconeogenesis. This in turn stimulates the uptake oflactic acid by the liver for conversion to pyruvate.Metformin inhibits gluconeogenesis, which prevents lactic acid from being removed from the blood by the lverand being converted to pyruvate for gluconeogenesis, This leads to increased circulating lactic acid.Metformin stimulates glycogenesis, which helps remove eecess glucose from the blood, lowering the amount oflactic acid in the blood.Metformin inhibits beta-oxidation, which decreases the amount of glucose needed and thus reduces the removalof lactic add from the blood.61

Name: 3 60Patients taking metformin are at increased risk of developing lact
Uploaded: 2024-03-20T06:42:55.000Z
Channel: Bartleby
Description: 3 60Patients taking metformin are at increased risk of developing lactic acidosis. How doesmetformin act to increase this risk?Metformin stimulates the consumption of pyruvate via gluconeogenesis. This in turn stimulates the uptake oflactic acid by t

Metformin can cause a hazardous condition called lactic acidosis. Individuals who have lactic…

Science

Biology

60 Patients taking metformin are at increased risk of developing lactic acidosis. How does metformin act to increase this risk? Metformin stimulates the consumption of pyruvate via gluconeogenesis. Thes in turn stimulates the uptake of lactic acid by the liver for conversion to pyruvate. Metformin inhibits gluconeogenesis, which prevents lactic acid from being removed from the blood by the liver and being converted to pyruvate for gluconeogenesis, This leads to increased drculating lactic acid. Metformin stimulates glycogenesis, which helps remove excess gluoose from the blood, lowering the amount of lactic acid in the blood. Metformin inhibits beta-oxidation, which decreases the amount of glucose needed and thus reduces the removal of lactic adid from the blood.

60 Patients taking metformin are at increased risk of developing lactic acidosis. How does metformin act to increase this risk? Metformin stimulates the consumption of pyruvate via gluconeogenesis. Thes in turn stimulates the uptake of lactic acid by the liver for conversion to pyruvate. Metformin inhibits gluconeogenesis, which prevents lactic acid from being removed from the blood by the liver and being converted to pyruvate for gluconeogenesis, This leads to increased drculating lactic acid. Metformin stimulates glycogenesis, which helps remove excess gluoose from the blood, lowering the amount of lactic acid in the blood. Metformin inhibits beta-oxidation, which decreases the amount of glucose needed and thus reduces the removal of lactic adid from the blood.

Nutrition Now

8th Edition

ISBN:9781337415408

Author:Brown

Publisher:Brown

Chapter7: How The Body Uses Food: Digestion And Absorption

Section: Chapter Questions

Problem 8RQ

See similar textbooks

Similar questions

A 9 year old mentally retarded girl with a protuberant abdomen, short stature, coarse facial features and cloudy corneas. skeletal malformations include dysostosis Multiplex and Bullet shaped middle phalanx .what is the enzyme deficient in this patient? A)Iduronate sulfatase B) beta - Galactosidase C)alpha - L- Iduronidase D) beta - Glucuronidase
Abnormal triglyceride accumulation in the liver (hepatic steatosis) leads to insulin resistance, which is trademark trigger of type 2 diabetes. Insulin-resistant hepatocytes perform gluconeogenesis even in the presence of high blood glucose levels, which exacerbates the hyperglycemia. These insulin-resistant cells also perform excessive b-oxidation, which can lead to ketoacidosis. Insulin normally suppresses lipolysis, and thus insulin-resistant adipocytes release too many fatty acids into circulation, many of which are taken up by hepatocytes and esterified into triglyceride. Thus, insulin resistance further exacerbates hepatic steatosis, which will in turn worsen insulin resistance in the liver. Given this vicious cycle, abatement of hepatic steatosis is one of the mainstays of diabetes treatment. Metformin is one such treatment and works by activating fatty acid degradation and inhibiting fatty acid synthesis. Which of the following could be the mechanism of action of metformin? (A)…
Administration of insulin decreases the blood concentration of ketone bodies in patients with diabetic ketoacidosis by which of the following mechanisms?A) Decreasing formation of ketone bodies in skeletal muscleB) Decreasing lipolysis in adipose tissueC) Increasing hepatic activity of carnitine acyltransferaseD) Increasing hepatic levels of acetyl CoAE) Increasing hepatic oxidation of ketone bodies
For the mutation of the enzyme, describe the effect it will have on carbohydrate metabolism. Also, make sure to think about the effect it has on muscles versus the liver: Mutation that converted the active site glutamate in phosphohexose isomerase to an glutamine.
This is a Biochemistry Question! Please select all of the following processes that would INCREASE during untreated or badly managed diabetic ketoacidosis: (More than 1 answer) 1) there is fluid and electrolyte loss in urine 2) plasma pH 3) Glucose uptake & skeletal muscle using as primary fuel 4) Bicarbonate reabsorption & renal Hydrogen excretion 5) Relying on fatty acids & proteins as primary fuels throughout the body 6) Gluconeogenesis, Fatty acid oxidation, & ketogenesis (all within the liver) 7) Lipolysis & fatty acid release from adipose
A patient has a defective liver FBPase-2 enzyme, the enzyme that converts F2,6P into F6P. This enzyme is inactive. What effect would this have on the differential regulation of glycolysis and gluconeogenesis in liver cells? How would this affect a person’s ability to respond appropriately to a low blood sugar state? What about a high blood sugar state?
Metabolic ketoacidosis is a common problem with diabetics, which is caused by which of the following? Excessive oxidation of fatty acids, leading to an accumulation of ketone bodies in the blood. Excessive oxidation of glucose, leading to an accumulation of ketone bodies in the blood. Excessive oxidation of proteins, leading to an accumulation of ammonia in the blood. Hyperglycemia.
Glucose 6-phosphatase deficiency is a glycogen storage disease referred to as von Gierke disease. Which of the following symptoms would you NOT expect to see in patients with this disease? (A) severe fasting hypoglycemia (B) excess adipose triglyceride storage and low circulating levels of fatty acids (C) hyperammonemia (D) liver enlargement resulting from excess liver glycogen storage (E) lactic acidosis (F) gout
A patient who has been drinking large amounts of alcohol for long periods of time shows thefollowing symptoms: apathy, loss of memory, and a rhythmical to-and-fro motion of the eyeballs.Which of the following reactions are most likely to be affected in the patient? A. Conversation of pyruvate to acetyl-CoA B. Conversation of a-ketoglutarate to succinyl-CoA C. Both A and B D. Neither A nor B
Mrs. Salma, a 55-year-old diabetic patient, experiences slow wound healing and peripheral neuropathy. Investigation reveals alterations in the Pentose Phosphate Pathway. How might dysregulation in the PPP contribute to complications such as slow wound healing and peripheral neuropathy in diabetic patients? Impaired nucleotide synthesis. Elevated insulin sensitivity. Lactic acid accumulation. Reduced oxidative stress.
Glucose can be made from oxaloacetate during gluconeogenesis, but if oxaloacetate concentrations are decreased,what other substance can be used to make glucose? How might this contribute to increased fat loss?
Choose which enzyme is likely deficient based on the symptoms described below: Elevated blood lactate, alanine and pyruvate a) lactate dehydrogenase d) citrate synthase c) pyruvate dehydrogenase d) pyruvate kinase