Results 71 to 80 of about 8,539 (162)

SGLT2 Inhibition Attenuates Renal Tubular Senescence by Suppressing CTRP1‐Mediated Glucotoxic Stress in Diabetic Kidney Disease

The FASEB Journal, Volume 40, Issue 14, 31 July 2026.
Hyperglycemia upregulates CTRP1 and SGLT2 in renal tubular cells, promoting glucose influx, CTRP1‐mediated glucotoxic stress, and tubular senescence in diabetic kidney disease. In the experimental model, SGLT2 inhibition with dapagliflozin was associated with reduced glucose uptake, attenuation of tubular senescence, suppression of CTRP1‐related ...
Lina Gu, Buhui Liu, Lei Zhang, Jing Zhao, Weiming He, Hong Lang, Wei Sun   +6 more
wiley   +1 more source

Generation of an induced pluripotent stem cell (iPSC) line from a patient with maturity-onset diabetes of the young type 3 (MODY3) carrying a hepatocyte nuclear factor 1-alpha (HNF1A) mutation

Stem Cell Research, 2018
Heterozygous non-synonymous (p.S142F) mutation in HNF1A leads to maturity-onset diabetes of the young (MODY) type 3, which is a subtype of dominant inherited young-onset non-autoimmune diabetes due to the defect of insulin secretion from pancreatic beta ...
Frank Griscelli, Hélène Ezanno, Mathis Soubeyrand, Olivier Feraud, Noufissa Oudrhiri, Amélie Bonnefond, Ali G. Turhan, Philippe Froguel, Annelise Bennaceur-Griscelli   +8 more
doaj   +1 more source

Cell Type‐Specific Roles of TBK1 in Steatotic Liver Disease: Evidence for an Inflammatory TBK1+CASP1+ Kupffer Cell State

Liver International, Volume 46, Issue 10, October 2026.
Yin Huang, Joanna Picó, Amalia Tzoumpa, Pedro Zapater, José M. González‐Navajas   +4 more
wiley   +1 more source

Mutations in HNF1A Result in Marked Alterations of Plasma Glycan Profile [PDF]

, 2013
A recent genome-wide association study identified hepatocyte nuclear factor 1-α (HNF1A) as a key regulator of fucosylation. We hypothesized that loss-of-function HNF1A mutations causal for maturity-onset diabetes of the young (MODY) would display altered
Klimes, Iwar, Rudd, Pauline M., Muzinic, Ana, Reynolds, Rebecca M., McCarthy, Mark I, Redzic, I., Mughal, Saima A, Redzic, Irma, Stanik, Juraj, Gyllensten, U, Kattla, JJ, Kattla, Jayesh J., Zgaga, Lina, Zgaga, L, Rudan, Igor, Kokic, I., Primorac, Dragan, Huffman, JE, Owen, Katharine R, Tjora, Erling, Strachan, M. W. J., Huffman, Jennifer E., Pucic, Maja, Wilson, J. F., Gasperikova, Daniela, Muzinic, A, Hassanali, N., Novokmet, M, Adamczyk, Barbara, Gasperikova, D, Wilson, James F, Hayward, C., Mughal, S. A., Hayward, Caroline, Adamczyk, B., Pedersen, Oluf B, Hansen, T, Klimes, I., Campbell, Harry, Campbell, H, Muzinic, A., Rudd, Pauline M, Gyllensten, Ulf, Hastie, Nicholas D, Wright, A. F., Wild, S. H., Nielsen, Trine, Thanabalasingham, G., Strachan, Mark W J, Kolcic, I, Bennett, Amanda J, Mughal, SA, Lauc, Gordan, Stanik, J, Reynolds, R. M., Pucic, M., Wright, AF, Njølstad, PR, Wild, SH, Bennett, Amanda J., Gloyn, A. L., Mughal, Saima A., Novokmet, Mislav, Strachan, Mark W. J., Zgaga, L., Wright, Alan F., Wright, Alan F, Polasek, Ozren, Rudd, PM, Polasek, O., Njolstad, P. R., Owen, K. R., McCarthy, M. I., Reynolds, RM, Njolstad, Pal R., Njølstad, Pål R, Wild, Sarah H; id_orcid, Kattla, Jayesh J, Huffman, J. E., Gyllensten, Ulf,, Campbell, Harry; id_orcid, Primorac, D, Klimes, I, Pucic, M, Nielsen, T., Stanik, J., Rudd, P. M., Wild, Sarah H, Gasperikova, D., Kolcic, Ivana, Novokmet, M., Redzic, I, Bennett, AJ, Rudan, I., Nielsen, T, Thanabalasingham, G, Hansen, Torben, Reynolds, Rebecca M, Wilson, JF, Essafi, A., Primorac, D., Wilson, James F., Rudan, I, Kattla, J. J., Strachan, MW, Thanabalasingham, Gaya, McCarthy, MI, Hastie, N. D., Wild, Sarah H., Gyllensten, U., Gloyn, Anna L, Campbell, H., Gloyn, Anna L., Owen, Katharine R., Gloyn, AL, Bennett, A. J., Hassanali, Neelam, Hayward, C, Essafi, A, Lauc, G., Pedersen, OB, Wilson, James F; id_orcid, Tjora, E, Hastie, ND, Essafi, Abdelkader, Huffman, Jennifer E, Hassanali, N, Gornik, O, Kokic, Ivana, Hayward, Caroline; id_orcid, Pedersen, Oluf B., Hastie, Nicholas D., Polasek, O, Lauc, G, McCarthy, Mark I., Gornik, Olga, Owen, KR, Adamczyk, B, Gornik, O., Gloyn, Anna, Tjora, E.   +140 more
core   +1 more source

Metastable Reprogramming State of Single Transcription Factor-Derived Induced Hepatocyte-Like Cells

Stem Cells International, 2019
We previously described the generation of induced hepatocyte-like cells (iHeps) using the hepatic transcription factor Hnf1a together with small molecules.
Seon In Hwang, Tae Hwan Kwak, Ji Hyun Kang, Jonghun Kim, Hyunseong Lee, Kee-Pyo Kim, Kinarm Ko, Hans R. Schöler, Dong Wook Han   +8 more
doaj   +1 more source

Serum levels of pancreatic stone protein (PSP)/reg1A as an indicator of beta-cell apoptosis suggest an increased apoptosis rate in hepatocyte nuclear factor 1 alpha (HNF1A-MODY) carriers from the third decade of life onward

BMC Endocrine Disorders, 2012
Background Mutations in the transcription factor hepatocyte nuclear factor-1-alpha (HNF1A) result in the commonest type of maturity onset diabetes of the young (MODY).
Bacon Siobhan, Kyithar Ma, Schmid Jasmin, Rizvi Syed R, Bonner Caroline, Graf Rolf, Prehn Jochen HM, Byrne Maria M   +7 more
doaj   +1 more source

Maturity onset diabetes of the young due to HNF1A variants in Croatia [PDF]

, 2018
Introduction: Maturity onset diabetes of the young due to HNF1A mutations (HNF1A-MODY) is the most frequent form of monogenic diabetes in adults. It is often misdiagnosed as type 1 or type 2 diabetes, but establishing genetic diagnosis is important, as
Šekerija, Mario, Burrows, CJ, Juszczak, A, McCarthy, MI, Agata Juszczak, Gloyn, Anna L, Amanda J Bennett, Mark I McCarthy, Pavić, T, Gloyn, Anna L., Owen, Katharine R., Ćuća Knežević, J, McCarthy, Mark I, Pape Medvidović, Edita, Gloyn, AL, Edita Pape Medvidović, Bennett, Amanda J, Pape Medvidović, E, Lauc, Gordan, Burrows, Carla, Katharine R Owen, Gornik, O, Tamara Pavić, Olga Gornik, Bennett, AJ, Bennett, Amanda J., Burrows, Carla J., Jadranka Ćuća Knežević, Lauc, G, McCarthy, Mark, Gornik, Olga, Mario Šekerija, Gordan Lauc, Pavić, Tamara, Owen, KR, Owen, Katharine R, Anna L Gloyn, Šekerija, M, Juszczak, Agata, Ćuća Knežević, Jadranka, Carla Burrows   +40 more
core   +1 more source

Maturity-onset Diabetes of the Young (MODY): How Much Can We Detect?

Bezmiâlem Science
Objective: This study aims to assess the characteristics of patients who underwent genetic analysis with suspicion of maturity-onset diabetes of the young (MODY). Methods: Forty patients who met the criteria of measurable serum fasting C-peptide levels,
Gökhan UYGUN, Akif AYAZ, Mustafa KANAT
doaj   +1 more source

Incidence of HNF1A and GCK MODY Variants in a South African Population

The Application of Clinical Genetics, 2020
Tandi E Matsha,1,* Shanel Raghubeer,1,* Abegail M Tshivhase,1 Saarah FG Davids,1 Gloudina M Hon,1 Lise Bjørkhaug,2 Rajiv T Erasmus1 1SAMRC/Cardiometabolic Health Research Unit, Department of Biomedical Sciences, Faculty of Health & Wellness ...
Matsha TE, Raghubeer S, Tshivhase AM, Davids SFG, Hon GM, Bjørkhaug L, Erasmus RT   +6 more
doaj  

A clinical case of pregnancy of a patient with a combination of two orphan diseases: familial partial lipodystrophy type 4 and HNF1A-MODY on the background of therapy with recombinant human methionyl leptin

Сахарный диабет
Lipodystrophies are a group of orphan diseases (according to different sources, the prevalence of the disease varies from 1 to 5 cases per 1,000,000 population), which can be either hereditary or acquired.
N. V. Frolkova, E. R. Radkevich, E. O. Koksharova, F. F. Burumkulova, P. A. Vasiliev, I. R. Minniakhmetov, I. A. Eremina, M. V. Shestakova   +7 more
doaj   +1 more source