Ottosson-Laakso Emilia, Tuomi Tiinamaija, Forsén Björn, Gullström Monika, Groop Per-Henrik, Groop Leif, Vikman Petter
Diabetes and Endocrinology, Department of Clinical Sciences, Lund University, Malmö, Sweden.
Folkhälsan Institute of Genetics, Folkhälsan Research Centre, Biomedicum, Helsinki, Finland.
PLoS One. 2016 Jan 6;11(1):e0146114. doi: 10.1371/journal.pone.0146114. eCollection 2016.
Familial renal glycosuria is an inherited disorder resulting in glucose excretion in the urine despite normal blood glucose concentrations. It is most commonly due to mutations in the SLC5A2 gene coding for the glucose transporter SGLT2 in the proximal tubule. Several drugs have been introduced as means to lower glucose in patients with type 2 diabetes targeting SGLT2 resulting in renal glycosuria, but no studies have addressed the potential effects of decreased renal glucose reabsorption and chronic glycosuria on the prevention of glucose intolerance. Here we present data on a large pedigree with renal glycosuria due to two mutations (c.300-303+2del and p.A343V) in the SLC5A2 gene. The mutations, which in vitro affected glucose transport in a cell line model, and the ensuing glycosuria were not associated with better glycemic control during a follow-up period of more than 10 years. One individual, who was compound heterozygous for mutations in the SLC5A2 gene suffered from severe urogenital candida infections and postprandial hypoglycemia. In conclusion, in this family with familial glycosuria we did not find any evidence that chronic loss of glucose in the urine would protect from deterioration of the glucose tolerance over time.
家族性肾性糖尿是一种遗传性疾病,尽管血糖浓度正常,但仍会导致尿液中出现葡萄糖排泄。它最常见的原因是编码近端小管中葡萄糖转运体SGLT2的SLC5A2基因突变。已经引入了几种药物作为降低2型糖尿病患者血糖的手段,这些药物靶向SGLT2从而导致肾性糖尿,但尚无研究探讨肾葡萄糖重吸收减少和慢性糖尿对预防葡萄糖不耐受的潜在影响。在此,我们展示了一个因SLC5A2基因中的两个突变(c.300-303+2del和p.A343V)而患有肾性糖尿的大家族的数据。这些突变在细胞系模型中影响葡萄糖转运,且在超过10年的随访期内,随之而来的糖尿与更好的血糖控制并无关联。一名SLC5A2基因杂合突变的个体患有严重的泌尿生殖系统念珠菌感染和餐后低血糖。总之,在这个患有家族性糖尿的家族中,我们没有发现任何证据表明尿液中葡萄糖的长期流失能防止葡萄糖耐量随时间恶化。