Assignment #4 - Article Review

Assignment # 4 - Article Review

Paper: Bobes, R. J., Castro, J. I., & Miranda, C. C. (2001). Insulin modifies the proliferation and function of chicken testis cells. Poultry Science, 80(5), 637-642

Paper can be retrieved from: http://ps.fass.org/content/80/5/637.full.pdf+html

Summary

As mentioned in the previous blogs, the main role of insulin is glucose homeostasis. However, it was also mentioned that insulin has several other roles such as stimulating lipogenesis, diminishing lipolysis, modulating transcription, and stimulating growth. 

Bobes et al. (2000) conducted an experiment to investigate whether insulin plays a role in the proliferation and the androgen production of chick testis cells since insulin is already present in the chick embryo. This is the first study to examine this. To see if insulin did in fact have an effect on chick testis cell proliferation and androgen production, Bobes et al. used testes from 18 day old chick embryos or newly hatched chicks. The testes were dissociated, the cells were pre-cultured and then cell suspensions were made and each were exposed to varying concentrations of insulin and human chorionic gonadotropin (hCG) for varying amounts of time. 

                                          Figure 1:  chick embryo at 18 days of development

Bobes et al. found that when incubated with insulin for one hour, the androgen production of the chick embryo testis cells was not directly affected. However, incubating the cells in insulin for an hour did modify how the cells responded to hCG in that it resulted in a slight but significant increase in androgen production. The opposite occurred when the concentration of insulin increased.  These results are shown in figure 1 of the paper.  On the other hand, the testes cells from the newly hatched chickens showed a large increase in the production of androgens (testosterone) with the addition of increasing dosages of insulin. These results are shown in figure 4.

Bobes et al. also found that insulin enhances the proliferation of embryonic cells by observing that insulin significantly increased the uptake of H-thymidine by testes cells as shown in figure 3 of the paper. 

In conclusion, the experiment shows that insulin does effect the proliferation and the androgen production of chick testis cells and that the stage of maturity affects the cells’ response to the hormone. It also demonstrates that insulin has a slight stimulatory on hCG-dependent androgen production in embryonic chick testis cells. 

Critique

Overall, the paper is well written. It is very easy to understand and is presented in an organized manner. The experiment is explained in a way that can be easily followed by the reader.  Also, the figures are very basic but effective at displaying the results of the experiment. I like that the paper did not include an overwhelming amount of statistical analysis. 

I would have liked a better explanation in the discussion as to why the embryo testes cells did not show an increase in the androgen production in the presence of insulin but the newly hatched chick testes cells did. Saying that sensitivity to insulin depends on stage of maturity seemed like an insufficient explanation.  

A little more background information in the introduction section would have aided in the understanding of the results obtained.

The results of the experiment did seem to support to the authors’ claims and it was interesting to read how the authors’ previous experiment tied in with the one conducted in this paper.

For future experiments, it is mentioned in the paper that while the results show that insulin does influence cell proliferation and androgen production of the chick testes cells, the mechanism of how this occurs needs further investigation. It would also be interesting to conduct this same experiment on another species to see if similar results are obtained.





*References can be accessed through links on pictures and citations.*

Assignment # 3 - The Function of Insulin

The Function of Insulin

The main function of insulin is glucose homeostasis. Insulin works to lower the amount of glucose in the blood. Insulin regulates the amount of glucose in the blood by causing cells in the liver, skeletal muscles and adipose tissue to take up glucose from the blood. In most nonhepatic tissues, insulin increases glucose uptake by increasing the number of plasma membrane glucose transporters: GLUTs. Glucose uptake in the liver is the result of an increase in the activity of the enzymes glucokinase, phosphofructokinase-1 (PFK-1), and pyruvate kinase (PK), the key regulatory enzymes of glycolysis (King, 2012). The glucose that is taken from the blood is stored as glycogen in the liver and muscles and as triglycerides in the adipose tissue.

A small amount of insulin is continuously secreted from the pancreas.  However, as blood glucose levels increase, this increase is detected by the glucose receptors located on the pancreatic beta cells which results in an increase in the amount of insulin being secreted from the pancreas.  As blood glucose levels return to normal then so does the secretion of insulin. Insulin is typically secreted immediately after eating a meal when carbohydrate levels are high. If glucose levels are low, the hormone glucagon is secreted which has opposing effects of insulin.

Figure 1: The control of glucose levels via the secretions of insulin and glucagon from the pancreas. 

While glucose homeostasis is the main function of insulin, it also has plays a role in several other processes including:

·         Stimulating lipogenesis

·         Diminishing lipolysis

·         Increasing amino acid transport into cells

·         Modulating transcription

·         Altering the cell content of numerous mRNAs

·         Stimulating growth

·         DNA synthesis

·         Cell replication

(Ramaraj, 2010) 

Insulin’s main role is to work to prevent hyperglycemia. Hyperglycemia is the medical term for high blood sugar.  Hyperglycemia affects people who have diabetes which can develop from a resistance to insulin or by the total lack of insulin secretion by the beta cells of the pancreas.

Type 1 Diabetes, also known as insulin dependent diabetes, occurs early in life.  In type 1 diabetes, the immune system attacks the insulin-producing beta cells in the pancreas and destroys them. This means the pancreas cannot secrete insulin or can only secrete insufficient amounts so the person ends up with hyperglycemia since there is not enough insulin produced to cause the uptake of glucose. Scientists do not know exactly what causes the body's immune system to attack the beta cells, but they believe that both genetic factors and viruses are involved (PHAC, 2010). While research is still ongoing, about 18 regions of the genome have been linked with influencing type 1 diabetes risk. These regions, each of which may contain several genes, have been labeled IDDM1 to IDDM18. The IDDM2 locus contains the insulin gene. Mutations of insulin gene cause a rare form of diabetes that is similar to MODY (Maturity Onset Diabetes in the Young). Other variations of the insulin gene (variable number tandem repeats and SNPs) may play a role in susceptibility to type 1 and type 2 diabetes (NCBI, 2004).

Type 2 Diabetes, also known as non-insulin dependent diabetes, is caused by the resistance of cells to the effects of insulin. Insulin can attach normally to receptors on liver and muscle cells but certain mechanisms prevent insulin from moving glucose into these cells where it can be used. Enough insulin is usually produced to overcome this resistance but eventually the pancreas will not be able produce enough to overcome the resistance. The resulting very high levels of blood glucose then beings to damage the beta cells of the pancreas and insulin secretion is halted completely (PHAC, 2010). While research is still ongoing, insulin resistance is thought to be due to the inheritance of a number of mutations in a variety of genes. Mutational analysis of the insulin signalling cascade has identified a glycine-arginine (Gly-Arg) substitution at codon 972 of the insulin receptor substrate-1 (IRS-1) gene associated with insulin resistance in obese individuals (Pedersen, 1990). 

Insulin injections are used to treat individuals with type 1 diabetes to aid in lowering blood glucose levels. Since individuals with type 2 diabetes have a resistance to insulin, treatment involves a change in diet that is low in glucose/carbohydrates. 

*References can be accessed through links on pictures and citations.*