Hi guys, this is a video which I was a part of for a group project. Please go to youtube to view the video and like it if you do! It describes the Gluconeogenesis processes and things you, the biochemian should know. Have a good one!
Please do go to the video on youtube….Your views contribute to us placing in the top 10 in the class. Thanks again
So, its been a while. Yes I know what some are thinking….. WHERE OH WHERE HAS CARLOS GONE!…Well he is alive, just barely. Just kidding. I’ve been preparing and writing my Final exams for the semester.
My blog took a little back seat for a while due to the load of assignments and laboratory exercises we had. In all the stress of things, my last exam is Tuesday 14th May which will be my exam for the course BIOL 1362, the course to which this blog assignment belonged to. To be very honest, I am grateful for the comments and emails that I have gotten throughout the semester from readers and fellow bloggers. This assignment was truly a great experience and the interaction with a global audience was great. It showed me that people out there in our great big world do care about the sciences and what I, as a student has to say about what I truly understand about a topic. It also made me feel (from the views and comments) that I was helping people understand a topic that they needed help with.
This isn’t a good bye….its more of a…..I’ll be around less often. I didn’t finish this assignment to the extent I wanted to. I still had to do some posts on TCA, ETC, Lipids and Nucleotic Acids but I didn’t. I WILL BE DOING IT SOONER OR LATER WITH A MONTHLY/FORTNIGHTLY UPDATE to THE BIOCHEMEFFECT.
To end this post, I’ll end it in good news….I got 9.3/10 for the blog assignment. YAY!!!!
I’ll like to thank my mom, my dad, my dog…wait I don’t have a dog…..but I will really like to thank my lecturer, Mr. Matthew for always being there to help us when we needed it……..Keep good now!
Hey guys, as part of my Blog assignment for my course BIOL1362, we had to include a video review on two topics covered. I chose as my second topic Enzymes in order to just give a general idea of what is on the web. Besides using my lecturer’s videos, I looked at many videos on YouTube. The title of the video I choose was Enzymes, by boozemanbiology. It caught my attention due it’s just above 11 minutes length. In this review I will analyze the video’s content.
The video firstly focused on the enzyme called catalase. Catalase is found in almost all living cells. Catalase breaks down hydrogen peroxide. Hydrogen peroxide is the substrate which feeds into the catalase and break down into H2O +O2.
According to the video an enzyme has an area called the active site. (This is the area where the substrate is going to fit in). As described, the active site is going to be part of the enzyme with a “hole” in it where the substrate fits in. This describes the Lock and key hypothesis. When the substrate fits into the active site there is going to be a “sort of tug” which will result in making it easier for chemicals to break off as describe. The tug is referred to as the lowering of the activation energy. The presenter further states that enzymes can be turn on or turn them off as described in the video.
Turning on the enzyme:
There are cofactors according to the video. This is small chemicals which are inorganic because they are not made up of carbon. Heme is an example of a cofactor. Coenzymes were also described. These are enzymes that act as a cofactor and help the enzyme to work. When cofactors and coenzymes are present only then the enzyme actually functions. If they are removed the enzyme stops.
Turning off the enzyme:
In trying to stop the substrate from binding, an inhibitor is used. Competitive inhibition was described as where another chemical/compound is used to bond with into the active site. If the bond occurs then the substrate cannot fit and the reaction will be stopped.
Allosteric inhibition is where it changes shape from the substrate. It is described as an inhibitor that bonds to the allosteric site and covers up the active site so that the substrate cannot bind.
Another method of allosteric inhibition is where the inhibitor bonds to the allosteric site and it changes the shape of the active site. There by the substrate will be unable to fit.
The video had information which I find very useful but some descriptions were very confusing. Firstly, there are more than 2 types of inhibition. The process of mixed inhibition and Un-competitive and Non-competitive inhibition was not mentioned. Furthermore, Allosteric enzymes change its conformation to fit the substrate and have more than one site to bind. The inhibition was confusing slightly in the video. This was not described accurately. For enzymes Video, I found it odd that the direct link to the Induce Fit Hypothesis and Lock and Key Hypothesis was not made. There could have been more examples when it came to the cofactors and coenzymes. A proper definition and processes should have been used. The presenter also spoke very fast. This made it hard to truly understand what he was saying. Overall the video was slightly okay in terms of content but lacked information crucial to the topic.
Hope this helps with studying
“Pharmacological potential of ampelopsin in Rattan tea.” ScienceDirect.com | Search through over 11 million science, health, medical journal full text articles and books.. Beijing Academy of Food Sciences, n.d. Web. 13 Apr. 2013. <http://www.sciencedirect.com/science/article/pii/S221345301200002X>.
Rattan tea is a traditional Chinese herbal remedy prepared from the stems and leaves of the plant Ampelopsis grossedentata. Ampelopsin is one of the most important flavonoids found in Rattan tea. The paper review summarizes current research related to the pharmacological functions and corresponding action mechanisms, as well as potential human health benefits of ampelopsin. Because of its reported effects, research into the bioactivity of ampelopsin in Rattan tea has gained increasing attention over the last decade, leading to increased understanding of its pharmacological functions and underlying mechanisms. Today, ampelopsin from Rattan tea is known for a broad range of biological functions including hypoglycemic, antioxidant and, anti-inflammatory, anti-tumor and hepatoprotective, and neuroprotective effects. As a dihydromyricetin (DMY), ampelopsin was first isolated from Ampelopsis meliaefolia by Kotake and Kubota in 1940, and was later reported as a major bioactive component in Ampelopsis grossedentata.
Ampelopsin in crude plant extracts has been applied to alleviate inflammatory diseases as a broad-spectrum anti-bacterial drug for several centuries. A structure–activity relationship analysis has indicated that the hydroxyl groups at 5 positions significantly enhanced the anti-inflammatory activity of ampelopsin. In addition, ampelopsin is also sensitive to inhibit other pathogenic microorganisms such as Aspergillus flavus, penicillium and transport streptavidin. Reports also indicated that ampelopsin exerts its anti-tumor effects by modulating multiple signaling pathways, including apoptosis, cell cycle arrest, cell growth inhibition and metastatic inhibition at various cellular levels. Currently, much attention has been paid to the anti-tumor activity of ampelopsin in cell and animal studies. A similar strong inhibitory effect on the growth of human hepatocellular carcinoma in mice has also been reported. The anti-metastatic effect of ampelopsin on melanoma and prostate cancer has been confirmed via in vivo and in vitro. In addition, reports suggest that ampelopsin may suppress angiogenesis by inhibiting the secretion of vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) from human hepatocellular carcinoma cells in vitro. Rattan tea has also had effects on regulation of proliferation and cell cycle arrest. It further inhibits the formation of apotosis by lowering the calcium content in the body, thereby fighting many cancers.
The research paper interest me due to the effect of Rattan tea as an inhibitor in many cases. It reduces the development of many diseases and aids in pharmaceutical treatment of other such disease. That research paper also highlights other effects it has which is rather interesting. Though used wildly, I personally have not heard of it. The plant and its effects are highly favourable and is used extensively in North-East of the world.
So, here is a little question for you guys 🙂
Enzymes form an Enzyme Substrate complex when interaction occurs with the Substrate. An Enzyme Substrate complex can be defined as;
A. the formation of readily bonded substrate to an active site
B. the chemical complex that is ionically form anywhere on the enzyme
C. a colour complex
D. the complex which the enzyme bonds to the substrate
E. the formation of readily bonded substrate to a complex formed.
Lieberman, Leslie Sue Lieberman. “Diabetes.” Credo Reference Home. Cambridge University Press, n.d. Web. 13 Apr. 2013. <http://www.credoreference.com/topic/diabetes
Diabetes mellitus (DM) is an endocrine disorder characterized by the lack or insufficient production of insulin by the pancreas. Insulin, a hormone produced in the pancreas by the islets of Langerhans regulates the amount of glucose in the blood. The lack of insulin causes a form of diabetes. DM has been recognized as a disease for at least two millennia, but only since the mid-1970s has there been a consensus on its classification and diagnosis. Symptoms include excessive urination, urine containing sugar, hunger, thirst, fatigue, and weight loss, are common to all types of DM.
The primary diagnostic criterion for DM is elevation of blood glucose levels during fasting or at 2 hours following a meal. Normal plasma glucose values for adults in the fasting state are 80–120 milligrams per deciliter (mg/dL). Definition of unequivocal DM requires a 2-hour postingestion plasma glucose level equal to or greater than 200 mg/dL for the appearance of classical symptoms of diabetes. Despite the use of a plethora of different terms in the past, diabetes is now generally classified as type I DM (insulin-dependent diabetes) and type II DM (non-insulin-dependent diabetes). Other variants of DM include maturity-onset diabetes of youth, tropical diabetes, which shows characteristics of both insulin dependence and nondependence, and gestational diabetes, which occurs during the latter part of pregnancy. Approximately 90–95 percent of all diabetics may be classified as type II, and about 5 percent as type I. Some 2 percent of diabetics have DM as a secondary result of other disease or injury.
Insulin-Dependent Diabetes Mellitus (Type I) Insulin-dependent DM is characterized by clinically acute onset, usually at an early age, reduction in the production and excretion of insulin, weight loss, thirst, frequent urination, and high levels of blood sugar. Some nutritional factors have been suspected of being involved in the etiology of type I diabetes, although there is no consistent picture. There is strong evidence for a genetic susceptibility, but of those individuals who carry the suspected antigens, only 30–50 percent develop DM; thus, environmental factors also appear to have a role. A number of studies indicate an increased prevalence of type I diabetes among populations that previously showed low rates. Excess caloric intake does not seem to be the important factor it is in type II diabetes. Typical type I diabetes is uncommon, affecting less than 0. 5 percent of the world’s population. Other possible causative factors include infectious viruses such as mumps, rubella, and meningitis. In general, these increases are associated with a “Westernization” of lifestyle since World War II.
Abundant worldwide evidence associates obesity with type II diabetes, and experts have concluded that it is the most powerful risk factor for non-insulin-dependent DM. However, it is difficult to disentangle the effects of decreased fiber consumption from increased sugar and carbohydrate intake, increased total calories, total fat, decreased caloric expenditure, and stresses associated with rapid dietary change and modernization. Conversely, during World War I and II in Europe and during World War II in Japan, when caloric intake was markedly decreased, obesity and diabetes both declined. It has been suggested that dietary fiber decreases the risk for diabetes, and different forms of fiber are being investigated in this connection. Genetic mechanisms interacting in complex ways with environmental factors are involved in the risk for type II diabetes. Diabetes rates have increased in a number of countries, such as Japan, Taiwan, Haiti, New Guinea, and parts of Africa, where caloric consumption per capita has also increased. Many causative factors have been implicated in type II diabetes and many observations have been made on sex differences in the frequency of type II diabetes. Most researchers agree that there is no convincing evidence that a single dietary component increases the risk of diabetes. More recent studies documented high frequencies of both obesity and diabetes among a number of Amerindian tribes in Oklahoma and in Latin American populations.
Tropical Diabetes, A type of diabetes found primarily in many tropical areas of the world has characteristics of both type I and type II. However, many areas show high rates of diabetes in populations that do not consume cassava, and some populations have high cassava consumption and low rates of diabetes. Risk factors for tropical diabetes involve unique dietary items. Information is relatively sparse on the genetics of diabetes in tropical countries. Recent studies have shown great population variability in increased susceptibility to diabetes. Genetic studies of Indian populations suggest a stronger familial factor among them compared to diabetics in other populations. For example, some types of cassava (manioc) may be toxic and produce pancreatic damage. In Kenya, a local alcohol called changaa is implicated in causing the disease. Finally, in most tropical areas carbohydrates constitute 70–80 percent of total calories, and such a diet is implicated in classic malnutrition diabetes because of low nutrient density and high fiber content.
In general, cities in the United States report a higher prevalence of gestational diabetes than do European cities. This form of the disease is difficult to distinguish from type II diabetes because a woman could have diabetes before pregnancy but not have it diagnosed until pregnancy. A type of diabetes present only during pregnancy was noted in 1882, which was Gestational diabetes. Babies born to diabetic mothers usually are large but may have immature organ systems, in which case they may not survive. However, it was not until the 1940s that the term “gestational diabetes” appeared in medical literature. The highest reported rate of gestational diabetes occurs among the Pima Indians of Arizona, who also have the highest prevalence of type II diabetes of any known population.
The publish paper from the University of Cambridge gives a historical side to diabetes. It does not go into any form of detail information on the chemistry of the disease but the implications. My reasoning for choosing this paper is due to the hormone Insulin. Insulin is a chemical messenger which contains several Amino Acids, 51 to be exact, which codes for its structure and function in the process. The document gives a brief over view of Diabetes but not the Biochemistry of it.