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#24438371 2014/01/17 To Up
Obestatin levels are associated with C-peptide and antiinsulin antibodies at the onset, whereas unacylated and acylated ghrelin levels are not predictive of long-term metabolic control in children with type 1 diabetes.Ghrelin secretion is altered at the onset and after the start of insulin therapy in children with type 1 diabetes. Contemporary regulation of acylated ghrelin (AG), unacylated ghrelin (UAG), and obestatin (OBST) remains undefined in this disease. It is unknown as to whether they could be good predictors of changes in glucose and metabolic control.
Flavia Prodam, Francesco Cadario, Simonetta Bellone, Letizia Trovato, Stefania Moia, Erica Pozzi, Silvia Savastio, Gianni Bona
2066 related Products with: Obestatin levels are associated with C-peptide and antiinsulin antibodies at the onset, whereas unacylated and acylated ghrelin levels are not predictive of long-term metabolic control in children with type 1 diabetes.0.1 mg100 μg0.1 mg100 μg1000 TESTS/0.65ml1000 1000 tests100 μg100ug Lyophilized100ul100 μg
#24127484 2013/10/14 To Up
Pathogenic CD4âº T cells recognizing an unstable peptide of insulin are directly recruited into islets bypassing local lymph nodes.In the nonobese diabetic mouse, a predominant component of the autoreactive CD4(+) T cell repertoire is directed against the B:9-23 segment of the insulin B chain. Previous studies established that the majority of insulin-reactive T cells specifically recognize a weak peptide-MHC binding register within the B:9-23 segment, that to the 12-20 register. These T cells are uniquely stimulated when the B:9-23 peptide, but not the insulin protein, is offered to antigen presenting cells (APCs). Here, we report on a T cell receptor (TCR) transgenic mouse (8F10) that offers important new insights into the biology of these unconventional T cells. Many of the 8F10 CD4(+) T cells escaped negative selection and were highly pathogenic. The T cells were directly recruited into islets of Langerhans, where they established contact with resident intra-islet APCs. Immunogenic insulin had to be presented in order for the T cells to localize and cause disease. These T cells bypassed an initial priming stage in the pancreatic lymph node thought to precede islet T cell entry. 8F10 T cells induced the production of antiinsulin antibodies and islets contained immunoglobulin (IgG) deposited on Î² cells and along the vessel walls.
James F Mohan, Boris Calderon, Mark S Anderson, Emil R Unanue
2053 related Products with: Pathogenic CD4âº T cells recognizing an unstable peptide of insulin are directly recruited into islets bypassing local lymph nodes.200ul100ul100 Tests96 assays200ul100ul100.00 ug1 mg250 TESTS0.1ml (1mg/ml)
#22854326 2012/07/31 To Up
Treatment of recurrent hypoglycemia with plasmapheresis and steroid in nondiabetic patient.We recently encountered a 35-year old man who suffered from frequent hypoglycemia. His blood test revealed the presence of high and suppressed level of insulin with supressed C-peptide levels, hypothalamic-pituitary axis was normal response in hypoglycemia and negative for anti-insulin antibody. Endocrinological and imaging data eliminated the possibility of insulinoma. His symptoms responded well to the therapy of prednisolone (60 mg/day) and plasmapheresis. We followed up the patient over the subsequent 6 months without remarkable lesions. He has had no further recurrences of hypoglycemia. We believe that the antiinsulin receptor antibody might have induced hypoglycemia in this patient.
Mustafa KulaksÄ±zoglu, Mustafa Sait Gonen, Levent Kebapcilar, Fatih Sahin, Fatih Demirci, Ali Topcu
2236 related Products with: Treatment of recurrent hypoglycemia with plasmapheresis and steroid in nondiabetic patient.100 assays100 MG100ug4 Arrays/Slide100ug1 Set1 Set1 Set
#20455202 2010/05/07 To Up
Green tea epigallocatechin gallate inhibits insulin stimulation of adipocyte glucose uptake via the 67-kilodalton laminin receptor and AMP-activated protein kinase pathways.Insulin and (-)-epigallocatechin gallate (EGCG) are reported to regulate obesity and fat accumulation, respectively. This study investigated the pathways involved in EGCG modulation of insulin-stimulated glucose uptake in 3T3-L1 and C3H10T1/2 adipocytes. EGCG inhibited insulin stimulation of adipocyte glucose uptake in a dose- and time-dependent manner. The concentration of EGCG that decreased insulin-stimulated glucose uptake by 50-60% was approximately 5-10âÂµM for a period of 2 h. At 10âÂµM, EGCG and gallic acid were more effective than (-)-epicatechin, (-)-epigallocatechin, and (-)-epicatechin 3-gallate. We identified the EGCG receptor [also known as the 67-kDa laminin receptor (67LR)] in fat cells and extended the findings for this study to clarify whether EGCG-induced changes in insulin-stimulated glucose uptake in adipocytes could be mediated through the 67LR. Pretreatment of adipocytes with a 67LR antibody, but not normal rabbit immunoglobulin, prevented the effects of EGCG on insulin-increased glucose uptake. This suggests that the 67LR mediates the effect of EGCG on insulin-stimulated glucose uptake in adipocytes. Moreover, pretreatment with an AMP-activated protein kinase (AMPK) inhibitor, such as compound C, but not with a glutathione (GSH) activator, such as N-acetyl-L-cysteine (NAC), blocked the antiinsulin effect of EGCG on adipocyte glucose uptake. These data suggest that EGCG exerts its anti-insulin action on adipocyte glucose uptake via the AMPK, but not the GSH, pathway. The results of this study possibly support that EGCG mediates fat content.
Chi-Fen Hsieh, Yi-Wei Tsuei, Chi-Wei Liu, Chung-Cheng Kao, Li-Jane Shih, Low-Tone Ho, Liang-Yi Wu, Chi-Peng Wu, Pei-Hua Tsai, Hsin-Huei Chang, Hui-Chen Ku, Yung-Hsi Kao