Chapter 9 Post

This chapter focuses on cell communication. Cell communication is defined as the process through which cells can detect and respond to signals in their environment. Cell communication is vital to our survival and involves an extraordinary diversity of signaling molecules and cellular proteins that are devoted to this process.


I actually find cell communication very interesting. This video shows an animation of cell communication. It was very well made and its explained very clearly. The major concept of cell communication is shown in a way that relates what we're learning to real life. Without cell communication, we wouldn't be here. Every bodily function relies on a myriad of signals from cell communication.

Apoptosis is programmed cell death. This article talks about leptin-deficient mice that are obese and infertile. The author believed dysfunctions of the ovaries were related to leptin-deficiency. Different mice with homozygote, heterozygote, or wild-type were obtained for analysis. The results were that compared with control ovaries with corpora lutea, ob/ob ovaries lacked corpora lutea, follicular atresia was at a higher rate; lipid droplets accumulated in follicle cells and in the oocyte with damaged mitochondria; the basement membrane of follicles was thickened. LOX-1 and CD36 expressions were comparable for all three groups. Ob/ob ovaries showed significantly higher levels of TLR4 and cleaved caspase-3 than the ones from the control groups. The high LC3-II/I ratio in the WT and ob/+ ovaries was related to the presence of corpora lutea. The StAR protein was lower in the ob/ob ovaries signifying reduced steroidogenesis. The conclusions were excessive lipid storage causes disorders of ovarian function in ob/ob mice. The local lipid overload leads to advanced follicular atresia with apoptosis and defect steroidogenesis. They suggest that the changes in lipid metabolism lead to increased oxidative stress and thereby, they are an important reason of anovulation and infertility.

This video shows signal transduction. It does a pretty good job of explaining everything and how its works. It gets relatively into detail without over analyzing signal transduction. It was sweet, simple, and got to the point.

 

Chapter 7 Post

This chapter covers cellular respiration and fermentation. Cellular respiration is a process by which living cells obtain energy from organic molecules and release waste products. Fermentation is the breakdown of organic molecules to harness energy without any net oxidation (that is, without any removal of electrons). 

One of the major focuses of this chapter is glycolysis. In glycolysis, glucose (a six carbon atom compound) is broken down to two pyruvate molecules (with three carbons each), producing a net gain of two ATP molecules and two NADH molecules. The two ATP are made by substrate-level phosphorylation, which happens when an enzyme directly transfers a phosphate from an organic molecule to ADP. Glycolysis occurs in the cytosol in eukaryotes. Initially, I found glycolysis a bit confusing. The ten steps can be overwhelming, but once I grasped the concept, it wasn't so bad. This animation explains all of the steps of glycolysis in a clear and concise manner. I found it much easier to learn glycolysis through animations than through pictures. Instead of just displaying the before and after, the animation demonstrated the process. The animation showed the structure changes and exactly what the enzymes did. I finally understood the isomerization of step 5 after watching the animation. The book didn't make it clear that fructose-1,6-biphosphate was split into dehydroxyacetone phosphate and glyceraldehyde-3-phosphate AND THEN dehydroxyacetone phosphate was isomerized (restructured) by isomerase (what a perfect name!) to make another molecule of glyceraldehyde-3-phosphate. I would suggest watching the animation for review on glycolysis.


The next step concerning the breakdown of glucose is the breakdown of pyruvate to an acetyl group. The two pyruvate molecules (from glycolysis) enter the mitochondrial matrix, where each one is broken down to an acetyl group (with two carbons each) and one CO2 molecule. One NADH molecule is made by the reduction of NAD+ for each pyruvate broken down via oxidation. I found this concept generally basic.

Subsequently comes the citric acid cycle! During the citric acid cycle (or the Krebs cycle), each acetyl group is incorporated into an organic molecule, which is later oxidized to liberate two CO2 molecules. One ATP, three NADH and one FADH2 are made in this process. Because there are two acetyl groups, the total yield is four CO2, two ATP via substrate-level phosphorylation, six NADH and two FADH2. This process occurs in the mitochondrial matrix. So not to bore you all with animations, but I found this animation helpful because it uses a ferris wheel analogy and it's interactive! As you can tell from my recent posts, I love interactive animations. But in this one, it actually makes you put the molecules in the correct order in the cycle. And if you get them wrong (I did my first try) it'll make you review and retry, so it's a good learning tool. Also, you get pop-up questions as well to make sure you understand everything.


Finally comes oxidative phosphorylation! Here, the NADH and FADH2 made in the three previous steps contain high-energy electrons that can be readily transferred in a redox reaction to other molecules. Once removed from NADH or FADH2 via oxidation, these electrons release some energy, and that energy is harnessed to produce a H+ electrochemical gradient. In the process of chemiosmosis, energy stored in the H+ electrochemical gradient is used to synthesize ATP from ADP and Pi. This process is called phosphorylation because ADP has become phosphorylated. About 30 to 34 ATP molecules are made via chemiosmosis. Oxidative phosphorylation is accomplished by two components: the electron transport chain and ATP synthase. I found this article from PubMed. It describes how muscle mitochondrial oxidative phosphorylation activity is altered with abdominal obesity in sedentary men. Abdominal obesity is a great risk factor for muscle insulin resistance. In the experiment, changes in muscle mitochondrial content and function were examined according to abdominal obesity and insulin sensitivity in men. The study was conducted on the general population of Clermont-Ferrand, France. The participants were forty-two healthy sedentary men between the ages of 37 and 45 years old. They were split into four groups according to waist circumference. Group 1's measurements were 87 cm or less, group 2 was between 88 and 93 cm, group 3 measured 94 to 101 cm and group 4's circumferences were 102 cm and greater. A plasma metabolic check-up was performed and insulin sensitivity index was calculated. In addition, muscle biopsies were obtained to assess mitochondrial content, oxidative phosphorylation activity and superoxide anion (reactive oxygen species) production. The results were that abdominal obesity was negatively correlated to the insulin sensitivity index and only group 4 was insulin-resistant. There weren't any between-group differences in muscle mitochondrial content and maximal activity of key oxidative enzymes. However, the muscle mitochondrial ADP-stimulated respiration rate was 24% higher in groups 2 and 3 compared to groups 1 and 4. Mitochondrial ATP and reactive oxygen species production rates were 27 and 48% lower in group 4 than in group 1. What does all of this mean? It means abdominal obesity is associated with alteration in intrinsic muscle mitochondrial function but not content. These adaptations mainly result in the reduced mitochondrial ATP production rate in response to insulin resistance. I liked how the article related what we are learning to a real life example. Most studies from PubMed are quite intricate and confusing, but I actually fully understood this one. That's an accomplishment for me.

So this concludes my chapter 7 post. Best of luck to everyone on the exam!