Home / Production Assistant, Diabetes In Control (page 2)

Production Assistant, Diabetes In Control


International Textbook of Diabetes Mellitus, 4th Ed., Excerpt #168: Molecular Genetics of Type 1 Diabetes Part 5

Linkage studies identify regions of the genome that are shared more frequently than would be expected by chance by relatives affected by a particular disease. Most studies analyze affected sibling pairs and utilize genetic markers that are scattered throughout the genome at moderate density, typically microsatellites. A significant excess of allele sharing identical by-descent (IBD) in affected sibpairs suggests that the region containing the marker locus also contains a disease susceptibility locus. The first linkage scan for T1DM identified 20 chromosomal regions with suggestive evidence of linkage to disease, including the HLA and INS gene regions.

Read More »

Consider More Accountability as a Treatment for Some Patients

Male, 57 years of age, type 2 diabetes. He started with us 6 months ago. When he started seeing us, he was taking  glipizide 10mg twice a day and metformin 1,000 twice daily for his glucose. His A1C was 7.5%, his BMI was 24. We stopped his glipizide and started him on a SGLT-2 and a weekly GLP-1. He met with the dietitian and made some big dietary changes, at least at the start. He also started wearing a CGM and was in our remote monitoring program. He sent me his CGM readings weekly for 4 months. He was doing so well, we decided he need not send me his weekly numbers but rather we’d review during his visits.

Read More »

International Textbook of Diabetes Mellitus, 4th Ed., Excerpt #167: Molecular Genetics of Type 1 Diabetes Part 4

The CTLA4 gene on chromosome 2q33.2 encodes a transmembrane co-receptor expressed on the surface of T cells. This functions as a negative regulator of T-cell activation via interaction with the B7 molecule on antigen-presenting cells (Figure 30.3). The G allele of the +49A/G SNP in exon 1 of CTLA4 has been implicated as a susceptibility marker for T1DM, but was rejected as a causal SNP by a fine-mapping study, which showed that its effect could be explained by more strongly associated variants in a 6.1 kb noncoding region, 3′ of the gene.

Read More »