A phenotypic characteristic, acquired during growth and development, that is not genetically based and therefore cannot be passed on to the next generation for example, the large muscles of a weightlifter. Any heritable characteristic of an organism that improves its ability to survive and reproduce in its environment.
Published December 6, By Dr. The most likely cause of the hypertriglyceridemia in this patient is which of the following? Deficiency in apoprotein C-II B. Increased hepatic triglyceride synthesis C. Decreased lipoprotein lipase activity D. Deficiency in LDL receptors E.
Absence of hormone-sensitive lipase. The correct answer is-C- Decreased Lipoprotein lipase activity. Circulating lipoproteins are just as dependent on insulin as is the plasma glucose, it is because, the lipoprotein lipase that catalyzes the degradation of circulating lipoproteins is activated by insulin.
Lipoprotein lipase Occurrence Lipoprotein lipase is located on the walls of blood capillaries, anchored to the endothelium by negatively charged proteoglycan chains of Heparan sulfate. It has been found in heart, adipose tissue, spleen, lung, renal medulla, aorta, diaphragm, and lactating mammary gland, although it is not active in adult liver.
Figure Action of lipoprotein lipase LpL. It is not normally found in blood; however, following injection of heparin, lipoprotein lipase is released from its heparan sulfate binding into the circulation. Hydrolysis takes place while the lipoproteins are attached to the enzyme on the endothelium.
Hypertriglyceridemia in Type 1 Diabetes Mellitus Dyslipidemia is a common metabolic abnormality in uncontrolled diabetes mellitus. Biochemical basis of dyslipidemia in uncontrolled DM One major role of insulin is to stimulate the storage of food energy following the consumption of a meal.
This energy storage is in the form of glycogen in hepatocytes and skeletal muscle. Additionally, insulin stimulates synthesis of triglycerides in hepatocytes and promotes their storage in adipose tissue.
In opposition to increased adipocyte storage of triglycerides is insulin-mediated inhibition of lipolysis insulin inhibits adipolysis because the enzyme hormone- sensitive lipase, that catalyzes adipolysis is stimulated by Glucagon and inhibited by Insulin.
The free fatty acids are taken up by numerous tissues however, not the brain and metabolized to provide energy. Free fatty acids are also taken up by the liver. Increased fatty acid oxidation Normally, the levels of malonyl-CoA are high in the presence of insulin. Mitochondrial oxidation of fatty acids generates acetyl-CoA which can be further oxidized in the TCA cycle.
These ketone bodies leave the liver and are used for energy production by the brain, heart and skeletal muscle. In IDDM, the increased availability of free fatty acids and ketone bodies exacerbates the reduced utilization of glucose furthering the ensuing hyperglycemia.
In diabetics, this can be easily diagnosed by smelling the breath. A spontaneous breakdown product of acetoacetate is acetone which is volatilized by the lungs producing a distinctive odor. Basis of hypertriglyceridemia Normally, plasma triglycerides are acted upon by lipoprotein lipase LPL.
In particular, LPL activity allows released fatty acids to be taken from circulating triglycerides for storage in adipocytes.
The activity of LPL requires insulin and in its absence a hypertriglyceridemia results figure Clinical pearls In type 1 diabetes, moderately deficient control of hyperglycemia is associated with only a slight elevation of LDL cholesterol and serum triglycerides and little if any change in HDL cholesterol.
Once the hyperglycemia is corrected, lipoprotein levels are generally normal. These smaller dense LDL particles are more susceptible to oxidation, which renders them more atherogenic. Measures designed to correct the obesity and hyperglycemia, such as exercise, diet, and hypoglycemic therapy, are the treatment of choice for diabetic dyslipidemia, and in occasional patients in whom normal weight was achieved, all features of the lipoprotein abnormalities cleared.
As regards other options Deficiency in apoprotein C-II Apo CII is an activator of lipoprotein lipase, but its concentration is not decreased in diabetes mellitus. Increased hepatic triglyceride synthesis The Acetyl Co A carboxylase, the key regulatory enzyme of fatty acid biosynthetic pathway, is activated by insulin, thus, de novo fatty acid synthesis is decreased in insulin deficiency.
However, the fatty acids mobilized from adipose tissue are used for esterification to form triglycerides which are transported from liver as VLDL. The excess flux of fatty acids that cannot be transported out as VLDL results in fatty liver.
The hypertriglyceridemia in uncontrolled DM can be because of excess hepatic triglyceride synthesis, but mainly it is due to non degradation of circulating chylomicrons carriers of dietary lipids and VLDL carriers of endogenous triglycerides by the inactive lipoprotein lipase figure Deficiency in LDL receptors LDL receptors internalize LDL, their deficiency cannot cause hypertriglyceridemia, and otherwise also, they are not deficient in diabetes mellitus.
Absence of hormone-sensitive lipase Hormone- sensitive lipase catalyzes the breakdown of triglycerides in adipose cells.Case details. A fifty-one year old woman presented to her internist with complaints of swelling In the front of her neck.
Upon history and physical examination, her physician noted that she had a weight gain in the past year of 28 pounds, had shortness of breath, and was easily fatigued. Metabolism: Metabolism, the sum of chemical reactions that take place in living cells, providing energy for life processes and the synthesis of cellular material.
Living organisms are unique in that they extract energy from their environments via hundreds of coordinated, multistep, enzyme-mediated reactions.
An endotherm (from Greek ἔνδον endon "within" and θέρμη thermē "heat") is an organism that maintains its body at a metabolically favorable temperature, largely by the use of heat set free by its internal bodily functions instead of relying almost purely on ambient heat.
Such internally generated heat is mainly an incidental product of the animal's routine metabolism, but under. Some people, even some scientists who study ketogenic metabolism, have the idea that ketogenesis is somehow abnormal, or exceptional; an adaptation for emergencies only.
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