Lipoprotein Lipase Lab Report

Dyslipidemia is a comorbidity in diabetes. Free relationship between hoisted triglycerides (TG), cardiovascular (CV) and mortality is to a great extent begging to be proven wrong. Lifted TG is associated with high thickness lipoprotein (HDL), low thickness lipoprotein (LDL) and different lipoproteins. Hypertriglyceridemia is connected with impressively expanded long haul mortality and cardiovascular danger. Relationships between's lower HDL cholesterol prompted contemplates prescribing that HDL qualities could be refered to as more probable benefactors to chance than the TG themselves. Grouping of hoisted TG as a noteworthy CV hazard component is thusly imperative since it manages whether high TG ought to be an objective for treatment. Sort 2 diabetes is classified by both insulin resistance and hyperinsulinemia. In hyperlipidemia patients, free unsaturated fats go about as forerunners to glycogenesis in the liver, in this manner expanding apoptosis in beta cells of the pancreas and expanding insulin resistance in muscles. This along these lines results in diminished insulin emission and tenacious hyperglycemia.

A higher level of fats in the body puts the patient at higher risk for Cardiovascular diseases(CAD). The patient's' family has a history of CAD. Her mom and one of her sister have CAD (Lewis et al., 2014, pp. 733-734). The patient states that she has been taking her meds for cholesterol atorvastatin regularly. Her lipase level was 8272 on 11/11/16 and 2829 on 11/12/16 U/L 1069 on 11/13/16 (Ref range 73-393 U/L). Her HDL cholesterol level was 21 ( ref range>49 mg/dl), LDL Cholesterol level 148 ( ref range: <130 mg/dL). Patient statin drug was on hold because it is contradicted on the patient with an elevated level of ALT 80, 61(Ref range 0-50 U/L) and AST 61 on 11/12/16 and 64 on 11/13/16 (ref range 0-45 U/L). The uncontrolled level of could be the cause of concern for stroke or acute myocardial

Dairy should not be a primary food group on the dietary guidelines set by the government because of its many negative effects on human health (given that people care about their health and the health of those around them). Dairy and other animal products are the only food sources which contain cholesterol. Arguments have been made saying that humans need to consume cholesterol in order to have a healthy balance of fats; these arguments fail to acknowledge that our bodies naturally produce all the cholesterol that it needs. And many studies have been conducted to support the theory that consumption of dietary cholesterol overloads arteries and can cause heart disease, artery disease, as well as sudden heart attacks. The Department of Community Health and Preventative Medicine at Northwestern University Medical School worked to interpret an international study based on data from the Food and Agriculture Organization and the World Health Organization. The overall conclusion was that “…dietary cholesterol levels are consistently related to CHD (coronary heart disease) mortality rates” (Stamler). A study conducted by Lena Ohlsson at the Laboratory of Gastroenterology and Nutrition within the prestigious Lund University in Sweden also linked dietary cholesterol and milk fat with artery disease and other metabolic disorders. In short, the abstract of her lab report said that low-density lipoprotein (LDL)—“bad” cholesterol—was found to be directly associated with coronary artery

My unknown organism #6 is Morganella morganii, which is a gram-negative bacillus rods commonly found in the environment and also in the intestinal tracts of humans, mammals, and reptiles as a normal flora. (3, 5) This bacterium Morganella morganii, was first discovered in the 1906 by a British bacteriologist named H. de R. Morgan. (2) Despite its wide distribution, it is an uncommon cause of community-acquired infection and is most often encountered inpostoperative and other nosocomial settings. (2, 3) Morganella morganii infections respond well to appropriate antibiotic therapy; however, its

Lactose is a sugar that can be put into smaller molecules, glucose and galactose. Lactose is when you are not able to digest milk and dairy meaning that the enzyme lactase that breaks down lactose is not functioning properly. ONPG was used as a substitute for lactase because even though it is colorless it helps show enzyme activity by turning yellow. This experiment measured the absorbance ONPG when exposed to lactase within an environment of different salinity’s. The enzyme, lactase, was obtained by crushing a lactaid pill and then was added into four cuvettes. ONPG and salt solution of different concentrations were added and their levels of absorption was measured by a spectrophotometer. The results showed that higher salt concentrations have a lower level of absorption. There were 4 cuvettes and within those cuvettes that solutions within them were being tested and the results showed the more salt solution added with the lactase the lower the absorbance. The less salt solution there was a higher rate of absorbance. The data supported the hypothesis that with increasing NaCl concentration there would be a decrease in enzyme activity.

According to the Merck Manual (2013), hyperlipidaemia is the increased synthesis of hepatic lipoproteins. Marieb (2012) explains that lipoproteins enable fat, fatty acids and cholesterol to circulate in the blood stream. They cannot do this alone due to their insolubility so they use lipoproteins as a type of transport. Nelson (2013) highlights four different varieties of lipoproteins which are chylomicrons, very low density lipoproteins (VLDL), low density lipoproteins (LDL) and high density lipoproteins (HDL).

In a study conducted in 1985 observing primates, it was determined that the major effect of dietary cholesterol is its LDL raising effects. High intakes of cholesterol increase the number of circulating LDL’s and it can also change its size and composition. [12] It was during this time period that the mechanisms by which SFA are thought to increase blood cholesterol concentrations came about. One mechanism for the increase in LDL cholesterol levels is the suppression of LDL receptor activity. Studies in tissue cultures have shown that increasing the cholesterol content of a cell will down-regulate synthesis of LDL receptors. [13] This will lead to an increase in concentration of blood cholesterol. Another cause for an increase in blood cholesterol concentration through intake of dietary SFA is the composition of the newly secreted lipoproteins. With a high saturated fat intake, the LDL’s become rich in cholesterol esters, leaving the triglycerides in the blood. [14] The use of non-human primates in

An Enzyme is a protein that in essence speeds up biological reactions. So that would mean that a Catalase is an enzyme reaction that decomposes hydrogen peroxide to water and oxygen. It is primarily found in the liver and it is important in protecting the cell from damaging oxidative reactions.

A change in the LIPE gene alters HSL leading to insulin resistance and diabetes. This happens when there is a normal level of insulin that is unused by the body. The body

According to kim et al. (2014), A 59-years-old man with account of alcohol addiction offered to an emergency room having dyspnea supplementary with diarrhea, malaise, a 40 pound weight loss and nausea for 4 months. He was hypoxic in ambulation. A CT of chest revealed borderline mediastinal lymphadenopathy. Lipase was raised to 1000. He was discharged numerous days once conservative treatment for recognized viral gastroenteritis, acute bronchitis, and pancreatitis. He improved to some extent but after three weeks, he returned to ER with persistent signs and a new-fangled bullous skin rash of his right ankle was found to be an eosinophillic vasculitis on skin biopsy. Moreover, He had a

“Reducing Risk in Heart Disease” (2012) indicate John has dyslipidaemia as low-density lipoprotein (LDL) levels of 5.6 mmol/L are above recommendation of 1.0 mmol/L and an increase of triglycerides (5.7) which should be <2.0. High LDL and low HDL are strong indicators for coronary risk. High triglycerides and total cholesterol level (9.4 mmol/L) is associated with coronary heart disease.

Lipoproteins are used to help deposit or remove types of lipids within the body. They have the job of transporting cholesterol and triglycerides which is within the blood. Lipoproteins reducing the cholesterol in the blood will help decrease the risk of types of heart diseases. High density lipoproteins have the job of removing all cholesterol from the walls. Low and very low-density lipoproteins work together to help deposit and reduce the narrowing of the arterial walls. The lipid profile test is used to help the personal trainer measure the cholesterol within the blood plasma. This can help the trainer monitor the client. The test helps to measure the risk of the clients getting coronary heart disease. There are three different ways to

FH can either be homozygous or heterozygous, homozygous being more rigorously affected than heterozygous. Heterozygotes have a plasma LDL concentration that is double that of normal individuals, thus increasing the risk of coronary artery disease. Atherosclerosis is the accumulation of white blood cells in the artery walls, thickening it over time. Individuals with two defective copies develop this disease at an early age which usually leads to death. It is always thought that FH is caused by the mutations of the LDL receptor proteins. There are currently more than 800 different mutations for the LDLR that cause FH (Soutar & Naoumova, 2007). The most common types of mutations are premature stop codons, mutations in the promoter and pre-mRNA, and amino acid substitutions. Individuals with autosomal recessive hypercholesterolemia have the same phenotype as the homozygous FH, but the conditions are not as extreme because of the cholesterol and LDL cholesterol levels. Treatment results show better results with lipid-lowering drugs. Some studies show that unaffected individuals and heterozygous individuals how no significant difference (Soutar & Naoumova, 2007). High cholesterol from birth will lead to vascular diseases and hardening of the

For this study on familial hypercholesterolemia, the primary populations utilized will be male and female adults roughly 25-65 years-old in the United States who have been diagnosed with heterozygous and homozygous FH. With more than 600,000 people in the United States having FH, and their children having a 50% chance of inheriting this disorder, it will be beneficial to focus on studies pertaining to those within our nation as a means to provide better care plans for those who are suffering from the disease and as a future means to work towards universal treatment of this disease.^7 In regards to sample inclusion/exclusion criteria, the articles will be those with available free full text, written in English, done with human

In our review, the core clinical feature of CGL was generalized fat loss noted during first 3 years of life and rarely during early adolescence (47). Supportive features included acromegaloid appearance, hepatomegaly (because of hepatic steatosis) (48), protuberant abdomen (due to organomegaly), and advanced bone age. Onset of DM was during early childhood through adolescence, except in a group of 10 Brazilian CGL patients homozygous for a 1036 bp deletion in the AGPAT2 gene (BSCL1 locus), as described by Gomes et al. (49) and a single patient in the NIH lipodystrophy database (age at onset of DM 34 years). Gomes et al. reported mean age at onset of DM as 25.67 ± 11.25 years in AGPAT2 group compared to 11.93 ± 8.29 years in BSCL2 (669insA Seipin) group (p=0.007) (49). Diabetes mellitus in CGL was ketosis-resistant, with higher insulin levels and higher insulin resistance reported in BSCL2 than in AGPAT2 patients (49).