Lecture 27-28NEW

Lecture 27-28NEW - 1 R.A. Luben Biochemistry120 June 2008...

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Unformatted text preview: 1 R.A. Luben Biochemistry120 June 2008 Reading: HORMONES; endotext.org; Online diabetes textbook: Chapters 5, 7, and 11 2 The liver in starvation and in diabetes 3 Diabetes: lack of insulin activity I n diabetes mellitus, insulin either is secreted in insufficient amounts or fails to act on its target tissues. Therefore, triacylglycerol hydrolysis, fatty acid oxidation, gluconeogenesis, and ketone body formation are accelerated and, in a condition termed ketosis , ketone body levels in the blood become abnormally high. Because glucose cannot enter muscle and fat cells, the glucose concentration in the blood rises even while the cells are reacting as they would in starvation. 4 Elevated levels of glucose and ketones can lead to a set of short-term life-threatening symptoms called keto-acidosis . I nsulin administration can control these. Long-term elevations of glucose also lead to damage in blood vessels, nerves, the immune system and the retina, leading to early death from a variety of problems (diabetic life-spans are decreased by 10-15 years on the average). Diabetic ketoacidosis I nability of glucose to enter fat and muscle cells causes these cells to break down triacylglycerols and glycogen. Lack of insulin in the liver prevents glycolysis and promotes gluconeogenesis, further increasing plasma glucose. Degradation of fatty acids in the liver produces excess ketone bodies. Hyperglycemia and ketosis are life threatening. Diabetic keto-acidosis 7 5 10 15 20 25 30 35 20-39 40-49 50-59 60-74 75+ Undiagnosed Diabetes Diagnosed Diabetes Impaired Fasting Glucose Age (yr) Percent of Population Prevalence of Diabetes and I mpaired Fasting Glucose, U.S., 1988-1994 Harris MI et al. Diabetes Care . 1998; 21:518-524. 9 Clinical development of Type 1 Diabetes The clinical onset of T 1 DM is preceded by development of antibodies against components of the pancreatic beta cell, leading to a process in which lymphocytes invade the islets and destroy most or all of the beta cells. The precipitating factor which causes the development of the autoimmune reaction is not known; in many cases there may be a viral infection (e.g. mumps, rubella) or other challenge to the immune system which begins the process. Age (years) Genetic Predisposition Beta cell mass (?Precipitating Event) Overt immunologic abnormalities Normal insulin release Progressive loss of insulin release Glucose normal Overt diabetes C-peptide present No C-peptide 12 Diabetes susceptibility genes Type 1 diabetes clearly has a heritable component. Families where one person has T1DM are more likely to have other cases....
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Lecture 27-28NEW - 1 R.A. Luben Biochemistry120 June 2008...

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