Diacyl Glycerol in the Context of Diabetic Nephropathy - Assignment Example

Question 1. Physiological Variable: DAG is involved in the growth urinary receptors which are responsible for relaxing the smooth muscle cells of the urinary bladder. This automates the nervous system leading to a change in physiological functions (Sherwood 121). 2. Mechanism of control: Ensures adequate cell signaling by using different messenger systems that act through specific effectors and censors to manage urine formation (Tripathi 184). 3. Cellular site of action: It has enzymatic activities which enable other intracellur systems to link with other proteins leading to appearance of insulin resistance in the kidneys (Sherwood 130). 4. Cellular action: DAG has the ability to activate inhibiting of other path ways like PKC not to be activated where signals are sent to other receptors and body systems to regulate uptake of amino acids by the body cells (Tripathi 177). 5. Cell signaling pathway: Diacyl Glycerol (DAG) 6.

Changes in Cell signaling pathway with age: DAG allows detection of any changes of cells in the urinary membrane due change in age (Sherwood 124). Generation of DAG in the kidneys causes subsequent changes to all cell types in the urinary track. 7. Pathophysiology due to a problem with the signaling pathway: DAG is an upstream deactivator of PKC, a pathway responsible for excessive formation of urine in the kidneys (Tripathi 176). When DAG is activated it ensures control of urine in the urine bladder by relaxing its muscles regularly.

The path way also acts as second messengers to kidneys receptors which signals other path ways. Question 2 Diabetic nephropathy is a serious diabetes complication characterized purposely by albuminuria and glomerular hyper filtration and it is one of the most known common sources of final stage of renal failure especially in the western world. It is characterized by massive growth of the extracellular matrix with coagulation of the tabular basement covering and the glomerular. Buildup of extracellular matrix proteins such a laminin, fibronectin and collagen are known to cause mesangial enlargement making most of the kidney cellular elements targets of hyperglycemic damage.

During hyperglycemia, the levels of glucose in the proximal tabular cells are increased causing DAG levels to increase (Tomino 16). The DAG accumulation leads to the activation of PKC and over production of TGF-β which may be a negative feedback of intracellur cell accumulation. Through the de novo amalgamation of diacylglycerol (DAG) protein kinase C is activated which leads to further activation of other intracellur indicators in transduction systems like the extracellular regulated kinase (ERK).

The activation of the three path ways: DAG, ERK and PKC are one of the most significant molecular mechanisms of the progression and development of diabetic nephropathy (Becker, Bilezikian, Bremner et al 957). By inhibiting the three paths there was prevention to development of glomerular dysfunction in diabetic people which proved the hypothesis that the three paths are important in diabetic nephropathy. Thiazolidinedione compounds inhibited PKC activation by ensuring that the DAG kinase was activated which prevented albuminuria, glomerular hyper filtration and the excessive manufacturing of extracellular matrix proteins for Type 1 diabetes.

Researchers have confirmed the significance of the activation of the three path ways in growth of glomerular dysfunction in diabetic nephropathy (Mohler 558). Work Cited Becker, Kenneth, John Bilezikian, William Bremner and Wellington Hung. Principles and Practice of Endocrinology and Metabolism. Philadelphia: Lippincott Williams & Wilkins, 2001. Mohler, Emile R. Advanced Therapy In Hypertension And Vascular Disease. New york: PMPH-USA, 2006. Sherwood, Lauralee. Human Physiology: From Cells to Systems.

New York: Cengage Learning, 2008. Tomino, Yasuhiko. Diabetic Nephropathy in Japan: From Bench to Bedside. Switzerland: Karger Publishers, 2001. Tripathi, G. Cellular And Biochemical Science. New Delhi: I. K. International Pvt Ltd, 2010.