DNA Polymorphisms as Disease Markers by Arno G. Motulsky (auth.), D. J. Galton, G. Assmann (eds.)

By Arno G. Motulsky (auth.), D. J. Galton, G. Assmann (eds.)

The goal of this workshop was once to evaluate the price of DNA polymorphisms for the prediction, analysis or elucidation of aetiology for universal metabolic illnesses similar to diabetes, hyperlipidaemia and atherosclerosis. the arrival of recombinant DNA concepts has produced an explosion in wisdom of limit web site polymorphisms and hypervariable sequences round candidate genes for such universal metabolic illnesses as atherosclerosis, hyperlipidaemia and diabetes mellitus. those illnesses are the key reasons of morbidity and mortality in Western societies this present day. for the reason that 1983 it has turn into obvious that there's even more version within the frequency and websites of those DNA polymorphisms in human populations than used to be before everything preferred and that almost all of those DNA polymorphisms are just linkage markers for the disorder. as a result it was once thought of well timed for laboratories fascinated about the mapping of those DNA mutations to satisfy jointly to debate the consequences in their stories. the most matters are no matter if such DNA polymorphisms will result in an identity of significant aetiological loci and that are the easiest concepts to accomplish this? what's the reason for the variations in frequencies of such polymorphisms among global populations? Are such reports top performed in homogeneous populations or in pedigrees? Are haplotypes, even though extra exhausting to build, a greater technique to continue than research of unmarried website polymorphisms? What are the consensus polymorphic websites that relate to the typical metabolic illnesses of diabetes, atherosclerosis and the hyperlipidaemias? the genuine want now to debate the theoretical history at the back of the

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First, the fraction of whole body glucose disposal that occurs via the splanchnic bed is insufficient to account quantitatively for insulin resistance in NIDDM. Second, the available data indicate that hepatic glucose uptake is not abnormal in type II diabetics [42]. Thus, ifthe liver/islet transporter is involved in the pathogenesis ofNIDDM, its effect is most likely at the level of the ~-cen. The major site of insulin resistance in NIDDM is skeletal muscle [42,43,44, Because GLUT 4 is the major insulin-responsive glucose transporter in this tissue, it is an excellent hypothetical target for a defect giving rise to insulin resistance (see Fig.

Studies of several of these pedigrees have demonstrated lack of linkage, suggesting that this locus is not involved in the pathogenesis of MODY (Permutt and Elbein, 1990). Linkage analysis in more typical NIDDM families was reported in Utah Mormons, representative of Northern European Caucasians (Elbein et ai, 1988b). Twelve families were informative for linkage, and lack of linkage was convincingly demonstrated in six. The conclusion of this analysis was that there was no linkage of the insulin gene and NIDDM under several models, and that insulin gene defects are not a major factor in the predisposition to NIDDM in Northern European Caucasians.

7. GLUT 1 and GLUT 4 mRNA levels in 3T3L1 adipocytes during glucose starvation. Steady-state levels of glucose transporter mRNAs were determined by northern blotting at various time points after withdrawal of glucose. Data from ref. 23. Ci3~ all 0:"2 - 6 to a. : 4 ..... c (I) CfJ c CIl C ..... " o 10 20 30 40 50 " "" /'1 60 70 80 Time After Glucose Withdrawal (Hr) Fig. 8. GLUT 1 and GLUT 4 protein levels in 3T3L1 adipocytes during glucose starvation. Glucose transporter protein levels were determined by Western blot analysis at various time points after glucose withdrawal.

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