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41.
Ronald S. Kaplan June A. Mayor Renee Blackwell Glenn L. Wilson Stephen W. Schaffer 《Molecular and cellular biochemistry》1991,107(1):79-86
The effect of non-insulin-dependent diabetes mellitus (i.e., NIDDM; type 2 diabetes) on the levels of functional mitochondrial anion transport proteins has been determined utilizing
a chemically-induced neonatal model of NIDDM. We hypothesized that moderate insulin deficiency exacerbated by the insulin
resistance, which is characteristic of NIDDM, would cause changes in mitochondrial anion transporter function that were similar
to those we have previously shown to occur in insulin-dependent diabetes mellitus (i.e., IDDM; type 1 diabetes) (Arch. Biochem. Biophys. 280: 181–191, 1990). Our experimental approach consisted of the extraction
of the pyruvate, dicarboxylate and citrate transport proteins from the mitochondrial inner membrane with Triton X-114 using
rat liver mitoplasts (prepared from diabetic and control animals) as the starting material, followed by the functional reconstitution
of each transporter in a proteoliposomal system. This strategy permitted the quantification of the functional levels of these
three transporters in the absence of the complications that arise when such measurements are carried out with intact mitochondria
(or mitoplasts). We found that experimental NIDDM did not cause significant changes in the extractable and reconstitutable
specific (and total) transport activities of the pyruvate, dicarboxylate, and citrate transporters. These results are in marked
contrast to our previous findings obtained using rats with IDDM and negated our hypothesis. The present results, in combination
with our earlier findings, allow us to conclude that insulin plays an important role in the regulation of mitochondrial anion
transporter function. Accordingly, in this model of NIDDM, where the level of insulin is not profoundly deficient, transporter
function is unaltered, whereas in IDDM, where a profound insulinopenia exists, transporter function is altered. Furthermore,
the present studies suggest that in the neonatal model of NIDDM the three mitochondrial transporters investigated are neither
affected by, nor are they the sites of the well documented hepatic post-receptor insulin resistance which is characteristic
of this disease. 相似文献
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Michael I. Lerman Farida Latif Gladys M. Glenn Lambert N. Daniel Hiltrud Brauch Shigeto Hosoe Krista Hampsch John Delisio Mary Lou Orcutt O. Wesley McBride Karl-Heinz Grzeschik Takashi Takahashi John Minna Patrick Anglard W. Marston Linehan Berton Zbar 《Human genetics》1991,86(6):567-577
Summary A collection of 2,000 lambda phage-carrying human single-copy inserts (> 700 bp) were isolated from two chromosome-3 flow-sorted libraries. The single-copy DNA fragments were first sorted into 3p and 3q locations and about 700 3p fragments were regionally mapped using a deletion mapping panel comprised of two humanhamster and two-human-mouse cell hybrids, each containing a chromosome 3 with different deletions in the short arm. The hybrids were extensively mapped with a set of standard 3p markers physically localized or ordered by linkage. The deletion mapping panel divided the short arm into five distinct subregions (A-E). The 3p fragments were distributed on 3p regions as follows: region A, 26%; B, 31%; C, 4%; D, 4% and E, 35%. We screened 300 single-copy DNA fragments from the distal part of 3p (regions A and B) with ten restriction endonucleases for their ability to detect restriction fragment length polymorphisms (RFLPs). Of these fragments 110 (36%) were found to detect useful RFLPs: 35% detected polymorphisms with frequency of heterozygosity of 40% or higher, and 25% with frequency of 30% or higher. All polymorphisms originated from single loci and most of them were of the base pair substitution type. These RFLP markers make it possible to construct a fine linkage map that will span the distal part of chromosome 3p and encompasses the von Hippel-Lindau disease locus. The large number of single-copy fragments (2,000) spaced every 100–150 kb on chromosome 3 will make a significant contribution to mapping and sequencing the entire chromosome 3. The 300 conserved chromosome 3 probes will increase the existing knowledge of man-mouse homologies. 相似文献