In Table 1 I have my substance of FAS,SREBP-1 and Actin and those are what I places in the wells of the gel to receive my results that I received in figure in Figure 5 picture F. If you compare me and my classmates primer optimization results, you can see that we all have a spear of the ladder on our gel. Another similarity is that we all did receive bands for FAS, SREBP and Actin and our cDNA came out very good with a dark band. Figure 6 is a repeat of Figure 5 picture F and the reason for repeating this experiment was because we were trying to see what other temperatures would work for Actin. Figure 7 is a western blot of SREBP-1c and it came out pretty nice. My cDNA was visible and the licor and Kal showed up very good and dark. My classmate actually performed the CPT-1 (Figure 8) western blot and you can barely see any bands for the cDNA but the actin and CPT-1 is very visible and it came out very dark. For the FAS (Figure 9) the licor and kal showed up very nice and bight red and there are bands for the cDNA visible and the Actin is visible as well. Fort he PPARα western blot, we have beautiful bands for the Cdna, Actin and the kal. If you compare Figures 7-10, you can see a resemblance in the kal, licor and Actin showing up better than the cDNA. If the cDNA is not showing up that well, maybe we need to increase the amounts of cDNA that we place in the wells. Figue 11 shows the PPARα western blot and Qpcr. For the western blot, there is no significant difference of protein PPARα but for the qPCR, the analysis shows that there is a significant increase in the IUGR compared to the control at approximately at 3 folds. For figure 12 western blot of PEPCK, there is a significant increase in the IUGR versus the control. For the PEP...
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...0.1055/s-2003-39781
4. White, Brett, MD. Dietary Fatty Acids. 8/2013. http://www.aafp.org/afp/2009/0815/p345.html. Los Angelas, CA. 80(4):345-350.
5. Brandt, Mark, Ph.D. Introduction to Lipid Metabolism. 2000-2003. http://www.rose-hulman.edu/~brandt/Chem330/Lipid_metab.pdf
6. Claudio Souza, Marisa Frederico, Gabriella Luz, Dennys Cintra, Eduardo Ropelle, Jose Pauli and Licio Vellosos. Acute exercise reduces hepatic glucose production through inhibition of the Foxo1/HNF-4α pathway in insulin resistant mice. 5/2010. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2911223/. 588(Pt12)
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7. No Author. Liver Function, Facts, Anatomy, and Disease. Web.2/2014. .
8. No Author. Metabolic Functions of the Liver. Web. 4/2014. http://www.vivo.colostate.edu/hbooks/pathphys/digestion/liver/metabolic.html.
9. Excel Graphing/Charting
The pathophysiology of type 2 diabetes is characterized by both insulin resistance and insulin secretion. Peripheral insulin resistance and inadequate insulin secretion by the pancreas due is due to beta cell dysfunction. The resistance results in elevated free fatty acids and inflammation which leads to an overall decreased amount of glucose taken up into the muscle, increased glucose production, and incr...
9. Zaharieva, D. P., & Riddell, M. C. (2013). Caffeine and glucose homeostasis during rest and exercise in diabetes mellitus. Applied Physiology, Nutrition & Metabolism, 38(8), 813-822.
Metabolic syndrome (MetS) is a combination of unfavo- rable health factors including abdominal obesity, dys- lipidemia, hypertension and glucose intolerance [1,2] and is strongly associated with increased risk of cardio- vascular disease (CVD) and type 2 diabetes [1,2]. One of the key drivers in the development of MetS is obesity [3]. In recent years, the global prevalence of obesity has increased at alarming rates, and MetS and its con- sequences have become a major public health burden [4,5]. This rise in MetS prevalence has also been ob- served in non-obese individuals [6-8] and there is strong evidence that the increase is mainly the result of un- favorable lifestyle changes, such as inactivity and poor nutrition [9].
Exercise can be used in conjunction to dietary control when diet alone is not maintaining appropriate glucose levels. The American Diabetes Association recommends participating in both aerobic (walking at a fast pace, swimming laps, playing tennis) and resistance training exercises (free weights or weight machines, resistance bands, wall-sits) .However, it is still controversial to endorse exercis...
Exercise is found to be the best at regulating the body's hunger response. The body fat that's used during exercise is consumed as fuel, which is a controlled burn. The body's chemicals of leptin, ghrelin, and insulin are kept on an even keel. All of this is regulated by the hypothalamus, which is always watching and waiting to read hunger signals.
"The Effect of Exercise on Homeostasis." LIVESTRONG.COM. LIVESTRONG.COM, 21 Oct. 2013. Web. 11 May 2014. .
Savage, P., Brochu, M., Poehlman, E., & Ades, P. (2003). Reduction in Obesity and Coronary Risk Factors After High Caloric Exercise Training in Overweight Coronary Patients. American Heart Journal, 146:317-23.
The purpose of this study, Pancreatic Mitochondrial Complex I Exhibits Aberrant Hyperactivity in Diabetes, is to establish that an increase of the stimuli in the pancreatic mitochondrial Complex I leads to diabetes. Increasing the stimuli of Complex I, subsequently raises the levels of reactive oxygen species and oxidative stress. Complex I, also known as NADH, is the first step of the respiratory electron transport chain which use protons to pump proteins creating most of the energy that helps power cells. This complex uses molecules to create an electrochemical gradient in our mitochondria, which is powered by the production of NADH by breaking down food molecules, helping to power ATP Synthase. Diabetes mellitus is a chronic disease in which the body’s ability to use energy produced by food intake is affected, causing an increased level of blood sugar. Hyperglycemia glucotoxicity is high blood sugar, which damages the structure and function of beta cells and target tissues of insulin, causing a low level of hormone secretion and insulin resistance.
Thus, the metabolic status during Emma’s fasted state entails that the blood glucose concentration was low and the insulin concentration in plasma was relatively low as well. With the low blood sugar levels, glucagon hormone was released and broke down the glycogen (glycogenosis) in the liver into glucose and some from glucose synthesis (gluconeogenesis). Glucose synthesis in the muscle was mobilized from alanine, lactate, and glycerol from the lipolysis of adipose tissues and was used within the muscle
Lebrausser, Nathan K. "'Weight Training' Reduces Fat And Improve Metabolism In Mice." Science Daily: News & Articles in Science, Health, Environment & Technology. Science Daily, 7 Feb. 2008. Web. 31 Mar. 2011. .
...hole-body insulin resistance in skeletal muscles (11, 32, 43). It should not be discounted though that the MR also has a high affinity for both aldosterone and 11β-hydroxy-glucocorticoids, which exist in lower levels in non-epithelial tissues that allow glucocorticoids to signal through the MR in cardiovascular and metabolic tissue such as skeletal muscle, liver and fat (72). Not a marginal point as insulin resistant populations have plasma glucocorticoid concentrations are greater than those of aldosterone and this may promote MR activation by glucocorticoids. Potentiating the oxidative stress in the cardio-renal metabolic syndrome (71). Indepdent of the in-/direct mechanism, the evidence of RAAS blockade or silencing can ameliorate oxidative stress, improves endothelial function and contributes to reductions of hypertension in the cardio-renal metabolic phenotype.
Glucose consumption in the tissues and glucose production are balanced when the body is at rest. At the start of exercising the energy the body gets quickly is from the anaerobic metabolism using mostly muscle glycogen...
Looking at today's habits, the functioning of our bodies indicates that everything is upside down. We start the day late, dress in a frenzy and fuel our bodies with a cup of sweetened coffee accompanied by a sugary snack to which our blood sugar counter starts to fail from skyrocketing levels. The blood sugar increase is still equal to insulin but now with our condition it's a truckload of insulin. Insulin's task is to escort the sugar in the blood to muscle cells, but since these cells have their own limits they do not want or need any more sugar than what is necessary. They actually become rude and resist taking that sugar from the blood. According to our biochemical pathway, the insulin now has no other choice than to take its sugar load to another location. It is an adventure story that doesn't bode well as it ends up in the fat cells. Our fat cells welcome the sugar, which is often under constant attack due to our high carbohydrate diets. Ev...
Immediately after a high carbohydrate meal, Insulin secrets rapidly due to glucose absorption into blood. This insulin act on many tissues in body and insulin turn causes rapid uptake, storage and use of glucose almost all issues of the body, but especially by the muscles, adipose tissue and liver. (8)
When a person exercises the body uses either sugar or fatty acids as fuel to create energy. During the beginning of an exercise most of the sugar that is used as fuel comes from the bloodstream or the muscles. After about 15 minutes the fuel starts to come from the liver. When one exercises after 30 minutes the body receives energy from free fatty acids and glycogen gets stored resulting in a decrease in blood sugar levels. Glycogen is the sugar stored in the liver and muscles.