BAFF-deficient (BAFFnull) and anti-BAFF antibody (Ab)–treated obese mice exhibit superior glucose metabolic control compared with WT and Bnull mice. BAFF-deficient.

Slides:



Advertisements
Similar presentations
Peter L. Lee, Yuefeng Tang, Huawei Li, David A. Guertin 
Advertisements

Volume 4, Issue 12, Pages (December 2015)
Question: Could diabetes be drivens by our bones?
Choosing a test of glucose metabolism in mice.
Volume 37, Issue 3, Pages (September 2012)
Volume 8, Issue 4, Pages (October 2008)
Volume 21, Issue 4, Pages (April 2015)
Irs1 Serine 307 Promotes Insulin Sensitivity in Mice
Volume 22, Issue 6, Pages (December 2015)
Volume 18, Issue 5, Pages (November 2013)
TFE3 prevents diet‐induced obesity and metabolic syndrome
Volume 17, Issue 5, Pages (May 2013)
Fig. 3. Fc fusion GDF15 molecules improve metabolic parameters in obese mice and obese cynomolgus monkeys. Fc fusion GDF15 molecules improve metabolic.
Impaired glucose tolerance in adult S1/3 KO mice on a normal chow
Volume 37, Issue 3, Pages (September 2012)
Volume 20, Issue 13, Pages (September 2017)
Antidiabetic Effects of IGFBP2, a Leptin-Regulated Gene
Improvement of insulin sensitivity by treatment of the annexin A1 receptor agonist in HFD mice. Improvement of insulin sensitivity by treatment of the.
Volume 23, Issue 4, Pages (April 2016)
The preventive role of TR in HFD‐treated mice
Volume 18, Issue 11, Pages (March 2017)
Volume 13, Issue 12, Pages (December 2015)
Volume 16, Issue 3, Pages (July 2016)
Therapeutic role of TR in HFD‐established diabetic mice
CD8+ T cells were immunomodulated and required for the efficacy of anti–4-1BB/anti–PD-1 combination treatment. CD8+ T cells were immunomodulated and required.
Hyperinsulinemic-euglycemic clamps revealed that obese TPL2KO mice have an improved insulin sensitivity compared with obese WT mice. Hyperinsulinemic-euglycemic.
Cyp8b1−/− mice have improved islet insulin secretion and increased islet insulin content but unchanged β-cell mass. Cyp8b1−/− mice have improved islet.
Overexpression of BTG2 resulted in an increase in hepatic gluconeogenesis. Overexpression of BTG2 resulted in an increase in hepatic gluconeogenesis. A:
NRP1-expressing macrophages accumulate in adipose tissue during DIO and regulate weight gain and glucose tolerance. NRP1-expressing macrophages accumulate.
Exogenous CRP administration causes fasting hyperglycemia and hyperinsulinemia without altering body composition. Exogenous CRP administration causes fasting.
1018-NT-β-cell clusters protect mice from STZ-induced diabetes.
WASH cKO mice display a normal pancreatic development.
TG-CRP mice display fasting hyperglycemia, hyperinsulinemia, and insulin resistance. TG-CRP mice display fasting hyperglycemia, hyperinsulinemia, and insulin.
GSIS. GSIS. In vivo: serum insulin levels at fasting state and 30 min after glucose injection (A) and the fold change in serum insulin after glucose loading.
FGF21 signaling in hypothalamus is blocked by FGFR1 neutralizing antibody. FGF21 signaling in hypothalamus is blocked by FGFR1 neutralizing antibody. Twelve-week-old.
GLUT4 LXRE is required for downregulation of adipose GLUT4 mRNA during fasting and diet-induced obesity. GLUT4 LXRE is required for downregulation of adipose.
Abberrent TGF-β activity causes impaired thermoregulation and excess adiposity in Mfap2−/− mice. Abberrent TGF-β activity causes impaired thermoregulation.
Modulation of insulin sensitivity by IL-6 in mice: A lack of PTP1B prevents chronic effects of IL-6. Modulation of insulin sensitivity by IL-6 in mice:
Loss of protection by linagliptin against obesity-related inflammation and insulin resistance in MIP-1α−/− mice. Loss of protection by linagliptin against.
Glucose tolerance in WT and TRPM2-KO mice.
Transgenic restoration of long-chain n-3 PUFA protects against obesity-linked insulin resistance and glucose intolerance. Transgenic restoration of long-chain.
At 6 months of age, PPARγ deletion in late osteoblast/osteocyte controls glucose homeostasis by increasing metabolic rate and glucose uptake in WAT, BAT,
ΑGLP-1R−/− mice show glucose intolerance and disturbed glucagon secretion in response to i.p. glucose administration. αGLP-1R−/− mice show glucose intolerance.
Insulin sensitivity in athletes and sedentary normal-weight and obese, young, and old individuals. Insulin sensitivity in athletes and sedentary normal-weight.
A: Chemical structure of pterosin A
ATL-801 treatment increases insulin sensitivity in KKAY mice.
Fig. 4 Deletion of hepatocyte HIF-2α does not affect obesity-induced glucose, glucagon, and insulin intolerance. Deletion of hepatocyte HIF-2α does not.
Chop deletion preserves β-cell function in P58IPK−/− mice.
Rapid improvement of glucose tolerance induced by PP
USP2–45 regulates hepatic gluconeogenesis.
SENP2 overexpression increases FAO by upregulating expression of FAO-associated enzymes in muscle. SENP2 overexpression increases FAO by upregulating expression.
Effect of anandamide on blood glucose clearance and insulin sensitivity. Effect of anandamide on blood glucose clearance and insulin sensitivity. A: Intraperitoneal.
HFD feeding induced insulin resistance in TRIB3 MOE mice.
Mice fed GP-SPI diet show improved fasting glucose and oral glucose tolerance. Mice fed GP-SPI diet show improved fasting glucose and oral glucose tolerance.
Hepatic PPARγ deficiency impairs the SCFA-induced reduction in hepatic steatosis. Hepatic PPARγ deficiency impairs the SCFA-induced reduction in hepatic.
Insulin resistance and hepatic steatosis in ASKO mice.
Treatment of high-fat diet–fed mice with TTR-ASOs decreases circulating TTR and RBP4 levels, and improves insulin sensitivity. Treatment of high-fat diet–fed.
MϕRIP140KD mice exhibit improved metabolic phenotypes.
Effects of Rosi treatment on ASKO mice.
Effects of chow-diet feeding on control and TRIB3 MOE mice.
Human IL-10 neutralization results in inhibited expression of intragraft Treg function genes and production of suppressive cytokine IL-10. Human IL-10.
Glucose-stimulated insulin secretion, plasma glucagon levels, and pancreatic hormone contents. Glucose-stimulated insulin secretion, plasma glucagon levels,
GTTs and ITTs. A: GTTs of WT (◇), LepTg (♦), Akita (open circles), and LepTg:Akita (closed circles) mice at 8 and 16 weeks of age. GTTs and ITTs. A: GTTs.
High-fat diet–induced glucose intolerance is prevented in ghrelin knockout (Ghr-KO) mice. High-fat diet–induced glucose intolerance is prevented in ghrelin.
Loss of Phb2 in β-cells induces development of diabetes over a 3-week period in β-Phb2−/− mice. Loss of Phb2 in β-cells induces development of diabetes.
Deficiency of adipocyte IKKβ does not affect diet-induced weigh gain but results in an exaggerated diabetic phenotype when challenged with an HFD. A: IKKβ.
Reduced tumor growth in CCR5-deficient mice is associated with perturbed killing ability of Treg cells. Reduced tumor growth in CCR5-deficient mice is.
Fig. 2 Loss of SBP2 induced inflammations in metabolically activated ATMs and inflammasome-associated IL-1β production. Loss of SBP2 induced inflammations.
Volume 26, Issue 1, Pages 1-10.e7 (January 2019)
Fig. 3. Effects of SFN in mice with diet-induced diabetes.
Presentation transcript:

BAFF-deficient (BAFFnull) and anti-BAFF antibody (Ab)–treated obese mice exhibit superior glucose metabolic control compared with WT and Bnull mice. BAFF-deficient (BAFFnull) and anti-BAFF antibody (Ab)–treated obese mice exhibit superior glucose metabolic control compared with WT and Bnull mice. Body weights (A), GTT with AUC (B), and ITT (C) of HFD WT, BAFFnull, and Bnull mice (n = 5). GTT with AUC (D), body weights (E), and fasting insulin (F) of HFD WT mice 4 weeks after they received anti-BAFF antibody or isotype control (n = 5). IgG concentration in serum (G) and VAT lysate (H) 5 weeks after anti-BAFF antibody treatment (n = 5). Cytokine concentrations in 24-h cultures of PerC (I) or spleen (J) cells stimulated with LPS from isotype control and BAFF antibody–treated mice (n = 5). K: mRNA expression in VAT from isotype control and BAFF antibody–treated mice (n = 4). Values are given as mean ± SEM. *P < 0.05; **P < 0.005; ***P < 0.0005. Lei Shen et al. Diabetes 2015;64:593-603 ©2015 by American Diabetes Association