Fads2−/− mice develop obesity resistance A–CBody size [cm] (nose‐tail root) and weight of male and female fads2−/− mice (age 4 months) differed by about.

Slides:

Advertisements

Similar presentations

Fig. 1. Body growth and leptin responsivity in young CPO and CTR mice

Advertisements

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

Figure Legend: From: High-Fat Diet–Induced Retinal Dysfunction

Volume 4, Issue 12, Pages (December 2015)

Question: Could diabetes be drivens by our bones?

Predictions of scaled weight based on lean body mass, fat-free mass,13 modified fat-free mass,16,17 ideal body weight, and pharmacokinetic (PK) mass14,15.

Volume 10, Issue 4, Pages (October 2009)

Volume 21, Issue 2, Pages (October 2017)

Prostaglandin E2 (PGE2) induces no significant alteration in circadian locomotor activity. Prostaglandin E2 (PGE2) induces no significant alteration in.

Statistical analysis of transgene expression in pigs generated by lentiviral gene transfer. Statistical analysis of transgene expression in pigs generated.

Morphology of white adipose tissue and muscle in S1/3 KO mice of different ages Morphology of white adipose tissue and muscle in S1/3 KO mice of different.

Amyloid‐associated gliosis in APPPS1‐21 transgenic mice.

Metabolic effects of TUG‐891 are reduced or absent in GPR120‐deficient mice Metabolic effects of TUG‐891 are reduced or absent in GPR120‐deficient mice.

JNK is activated by Wnt5a.

Measurement of terminal restriction fragments (TRFs) in bone marrow cells from both parents and the G4 progeny. Measurement of terminal restriction fragments.

TRF2ΔBΔM induces apoptosis and senescence in the mouse liver.

Cognitive deficits in APPPS1‐21 mice.

The gene encoding TP53INP1 is expressed in pancreatic endocrine cells A, B(A, B) Immunocytofluorescent staining of TP53INP1 (red) and insulin (green) in.

Volume 3, Issue 1, Pages (July 2002)

Volume 21, Issue 5, Pages (May 2015)

PPARγ is SUMOylated at K107 in WAT

Topological overlap matrix (TOM) plots of weighted, gene coexpression networks constructed from one mouse studies (A–F) and four human studies including.

TFE3 regulates glucose homeostasis

AAV8‐hAAT‐FGF21 treatment improves liver fibrosis

Metabolic profile of Tfe3 KO mice fed a HFD

Volume 21, Issue 2, Pages (October 2017)

Volume 20, Issue 4, Pages (October 2014)

Metabolic profile of Tfe3 KO mice

Wdr11 knockout mouse shows neuroendocrine and metabolic dysfunctions

Volume 21, Issue 11, Pages (December 2017)

Volume 14, Issue 3, Pages (September 2011)

TFE3 prevents diet‐induced obesity and metabolic syndrome

Impaired glucose tolerance in adult S1/3 KO mice on a normal chow

Negligible T22‐GFP‐H6‐FdU biodistribution or toxicity on non‐tumor tissues Negligible T22‐GFP‐H6‐FdU biodistribution or toxicity on non‐tumor tissues AUndetectable.

Combination of OTX‐015 and PD does not induce overt toxicity

Molecular and clinical characterization of AAV2/8‐TBG‐h

Age‐related amyloid deposition in APPPS1‐21 mice.

Protection against High-Fat-Diet-Induced Obesity in MDM2C305F Mice Due to Reduced p53 Activity and Enhanced Energy Expenditure Shijie Liu, Tae-Hyung.

Volume 14, Issue 10, Pages (March 2016)

Intra‐eWAT administration of FGF21 vectors in ob/ob mice

Circadian Disruption Leads to Insulin Resistance and Obesity

Treatment with AAV8‐hAAT‐FGF21 improves insulin sensitivity and glucose tolerance Treatment with AAV8‐hAAT‐FGF21 improves insulin sensitivity and glucose.

Volume 10, Issue 1, Pages (July 2009)

The preventive role of TR in HFD‐treated mice

Volume 13, Issue 12, Pages (December 2015)

GPR120 deficiency alters the expression of genes involved in glucose and lipid metabolism in BAT GPR120 deficiency alters the expression of genes involved.

Target engagement of the systemic Stat3 inhibitor in APP/PS1 mice

High-Fat Diet Triggers Inflammation-Induced Cleavage of SIRT1 in Adipose Tissue To Promote Metabolic Dysfunction Angeliki Chalkiadaki, Leonard Guarente

Absence of a vestibular phenotype in CIB2−/− mice

Tangle formation and downregulation of miR‐132‐3p in LOAD A‐G

Volume 24, Issue 12, Pages (September 2018)

Fig. 2. Body weight and size analysis of A1/A2-KO mice

Fig. 1. Body weight gain in Cbx7-KO mice

Cellularity of epididymal adipose tissue.

Loss of protection by linagliptin against obesity-related inflammation and insulin resistance in MIP-1α−/− mice. Loss of protection by linagliptin against.

Transgenic restoration of long-chain n-3 PUFA protects against obesity-linked insulin resistance and glucose intolerance. Transgenic restoration of long-chain.

Effect of berberine on white adipose tissue mass.

At 6 months of age, PPARγ deletion in late osteoblast/osteocyte controls glucose homeostasis by increasing metabolic rate and glucose uptake in WAT, BAT,

Chop deletion preserves β-cell function in P58IPK−/− mice.

Metabolic parameters of Id1−/− and wild-type mice fed a standard chow diet (hatched bars and striped bars, respectively) or a high-fat diet (black bars.

MϕRIP140KD mice show browning in vWAT.

Insulin resistance and hepatic steatosis in ASKO mice.

Effects of Rosi treatment on ASKO mice.

Effects of chow-diet feeding on control and TRIB3 MOE mice.

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.

SORCS1 and SORCS3 control energy balance and orexigenic peptide production Representative hematoxylin and eosin (H&E)‐stained sections of perigonadal white.

Fig. 3. Differences in the prevalence of albuminuria after comorbidity stratification. (A) Obesity defined by a body mass index ≥25 kg/m2, (B) central.

Volume 26, Issue 1, Pages 1-10.e7 (January 2019)

Fig. 1 Obesity-related adipocyte degeneration and cfDNA release.

Volume 6, Issue 6, Pages (December 2007)

Presentation transcript:

Fads2−/− mice develop obesity resistance A–CBody size [cm] (nose‐tail root) and weight of male and female fads2−/− mice (age 4 months) differed by about 20 and 25% from control +/+ mice (A, B), similarly of female DHA−/−, unlike those of AA−/− (n = 20) (C). Fads2−/− mice develop obesity resistance A–CBody size [cm] (nose‐tail root) and weight of male and female fads2−/− mice (age 4 months) differed by about 20 and 25% from control +/+ mice (A, B), similarly of female DHA−/−, unlike those of AA−/− (n = 20) (C). D, ENMR‐spectroscopy revealed significantly reduced% fat mass (D) and correspondently elevated% lean mass of body weight in fads2−/− (n = 10) (E). FWet weight [g] of WAT of fads2+/+ and AA+/+ (black bars) was four and three times and of BAT about twice higher than that of corresponding fads2−/− mice. Weight of WAT and BAT of DHA−/− exceeded twice that of DHA+/+ mice (n = 10). Liver weight of nd‐, AA‐ and DHA+/+ mice was 1.3, 1.5 and 1.2 times higher than that of corresponding fads2−/− mice. G, HIn HE‐stained sections (5 μm) epididymal adipocytes of nd+/+ were significantly larger than epididymal adipocytes of nd−/− mice, about three times in AA‐ and twice in DHA+/+ mice. IGlucose tolerance test (GTT) (15 min P = 0.0342, 30 min P = 0.0019, 60 min P = 0.0130, 120 min P = 0.0271) of nd‐fads2+/+ and −/− mice (red). JInsulin tolerance test (ITT) (15 min P = 0.030, 30 min P = 0.0001, 60 min P = 0.0005, 120 min P = 0.030) of nd‐fads2+/+ and −/− mice (red). KNormal GTT of AA+/+ and AA−/− mice (n = 10). LNormal ITT of AA+/+ and AA−/− mice (n = 10). MGTT of DHA+/+ and DHA−/− mice (n = 10). NITT of DHA+/+ and DHA−/− mice (n = 10). Wilhelm Stoffel et al. EMBO Rep. 2014;15:110-120 © as stated in the article, figure or figure legend