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What about other aspects of metabolic syndrome? Is fructoseimplicated in increased fat storage in the liver and for thedevelopment of non-alcoholic fatty liver disease?

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Patrina Schowalter
Patrina SchowalterLv2
29 Sep 2019
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Related questions

In the 90’s, one new way to treat patients with HIV was by administering growth hormone in order to combat the muscle wasting that is associated with this disease. Growth hormone administration worked very well in reducing muscle loss but it had an unfortunate side effect: it caused diabetes in the people treated. By which mechanism is growth hormone likely causing diabetes?

a)

Growth hormone causes decreased adipose tissue free fatty acid release, increased skeletal muscle glucose uptake and increases liver gluconeogenesis
b)

Growth hormone causes decreased adipose tissue free fatty acid release, decreases skeletal muscle glucose uptake and decreases liver gluconeogenesis
c)

Growth hormone causes increased adipose tissue free fatty acid release, decreases skeletal muscle glucose uptake and increases liver gluconeogenesis
d)

Growth hormone causes increased adipose tissue free fatty acid release, increases skeletal muscle glucose uptake and increases liver gluconeogenesis

In your research you are analyzing the changes in liver gene expression in a mouse model of non-alcoholic fatty liver disease. You previously performed microarray analysis on livers of mice given a high-fat diet verses mice on regular diet and found a number of genes that were abnormally expressed in the high-fat diet mice. You perform quantitative RT-PCR on some of these genes and receive the following Ct values:

high-fat diet: Gapdh-10, Cyp8b1-27, Cyp17a1-25, Asns-21, Past1-23.

Regular diet: Gapdh-11, Cyp8b1-25, Cyp17a1-21, Asns-26, Past1-30.

Question a: For each of the genes, complete calculations using the delta-delta Ct method to determine the relative fold change in gene expression for the mice with the high-fat diet. (hint use Gapdh as the reference gene and SHOW YOUW WORK).

Question b: Which of the four genes are up-regulated and which of the four genes are down-regulated in mice with high-fat diets?

Question c: You want to determine exactly where in the liver these genes are normally expressed. Pick one of the genes above and design an experiment to perform in livers of high-fat diet mice and regular diet mice (as a control) to determine the location of the gene expression in the liver. Describe the results you expect to see from this experiment in the two different mouse livers.

Question d: You hypothesize that the change in expression of the gene you picked in part C. Above is a result of differences in epigenetic marks. Briefly describe what changes in epigenetic marks at this gene's locus are expected to occur as a result of the high-fat diet. In your answer address both DNA methylation and histone modifications.


Key: SD, standard diet; LF, low fat diet; KG, high fat (carbohydrate restricted-no carbs); HF mix, high fat + high carbohydrate “Western Diet”. BHB-CoA, beta-hydroxybutyryl-CoA; AcAc-CoA, acetoacetatoyl-CoA. Data are from livers (post absorptive) collected from rats fed the diets for three weeks.

a)Which major lipid pathway (s) do these intermediates reflect

Panel A._____________________________

Panel C._______________________________

b) What is the key enzyme (rate limiting step) for fatty acid synthesis ?________________________

c) How is this enzyme (in Q1 b) regulated in the fed vs fasted state in Liver?

What are the major differences in the regulation beta-oxidation in Muscle compared to liver?

Discuss prevention of futile cycles between fatty acid synthesis and beta-oxidation in liver and include transporter system (4 key regulatory steps & regulation) between cytosol and mitochondria.

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