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Leptin but not its long form receptor regulates intestinal membrane expression of sodium/glucose transporter‐1 and intestinal hyperplasia
Author(s) -
Rieg Jessica A Dominguez,
Gerasimova Maria,
Koepsell Hermann,
Rieg Timo
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.1210.13
Subject(s) - medicine , endocrinology , leptin , leptin receptor , crypt , chemistry , receptor , hyperplasia , small intestine , biology , obesity
Small intestinal hyperplasia occurs in type 2 diabetic conditions and is associated with alterations in intestinal Na+/glucose transporter 1 (SGLT1) abundance. To study the role of leptin and its receptor in intestinal hyperplasia and expression of SGLT1, we utilized leptin‐receptor (LEP‐R) deficient mice with compensatory increased leptin levels (db/db; n=6), leptin‐deficient mice (ob/ob; n=5), and their controls (db/con and ob/con, n=10 and 6, respectively). Db/db and ob/ob were obese (46±1 vs 27±2 g and 46±1 vs 25±1 g, respectively; P<0.01 ) and hyperglycemic (532±24 vs 120±4 mg/dl and 315±34 vs 168±9 mg/dl, respectively; P<0.01 ) vs con. Both db/db and ob/ob had longer small intestines vs controls (37±2 vs 30±1 cm and 37±1 vs 32±1 cm, respectively; P<0.01 ). Db/db had longer villi (673±14 vs 483±20 μm; P<0.01 ) and deeper crypts (112±2 vs 98±3 μm; P<0.01 ) vs db/con. In contrast, ob/ob and ob/con had comparable villi lengths (416±15 vs 397±6 μm; P=NS ) and crypt depths (63±3 vs 70±2 μm; P=NS ). In db/db, immunofluorescence revealed SGLT1 apical membrane abundance was nearly absent and SGLT1 protein expression was decreased vs db/con (44%±10 vs 100%±8; P<0.01 ). In contrast, apical membrane abundance in ob/ob vs ob/con was not different. Increased leptin levels in type 2 diabetes may regulate intestinal glucose transporter abundance independent of the long form of the LEP‐R and may contribute to intestinal hyperplasia.