1-20 of 872 Search Results for

wat-white-adipose-tissue

Follow your search
Access your saved searches in your account

Would you like to receive an alert when new items match your search?
Close Modal
Sort by
Meeting Abstracts
Journal: Diabetes
Diabetes 2019;68(Supplement_1):282-LB
Published: 01 June 2019
... (follistatin) secreted by the liver of LDKO-mice inhibits insulin action in WAT (white adipose tissue) and promotes hepatic glucose production; however, Fst does not dysregulate BAT (brown adipose tissue). Regardless, BAT in LDKO-mice lacked typical BAT characteristics on the anatomical and molecular level...
Images
Central nesfatin-1/NUCB2 knockdown decreases glucose utilization in <span class="search-highlight">tissues</span>...
Published: 13 March 2014
Figure 4 Central nesfatin-1/NUCB2 knockdown decreases glucose utilization in tissues. A: Hyperinsulinemic-euglycemic clamp procedure. Glucose utilization was assessed in gastrocnemius and soleus muscle tissue (B), interscapular BAT (C), and WAT (D). n = 4. *P < 0.05, **P < 0.01 vs. NCA group; ▲P < 0.05 vs. HFA group. BAT, brown adipose tissue; WAT, white adipose tissue. Figure 4. Central nesfatin-1/NUCB2 knockdown decreases glucose utilization in tissues. A: Hyperinsulinemic-euglycemic clamp procedure. Glucose utilization was assessed in gastrocnemius and soleus muscle tissue (B), interscapular BAT (C), and WAT (D). n = 4. *P < 0.05, **P < 0.01 vs. NCA group; ▲P < 0.05 vs. HFA group. BAT, brown adipose tissue; WAT, white adipose tissue. More
Images
Human adult “brown fat” has the molecular signature of beige <span class="search-highlight">adipose</span> cells....
Published: 17 May 2013
FIG. 16. Human adult “brown fat” has the molecular signature of beige adipose cells. Biopsies of human PET-positive brown fat and neighboring white fat depots were taken, and RNA was prepared. qPCR was performed for UCP1 and beige and brown selective mRNAs. For further details, see ref. 16 . BAT,... More
Images
Pericentrin expression in human and murine <span class="search-highlight">tissues</span>. <em>Pcnt</em> m...
Published: 21 February 2011
FIG. 4. Pericentrin expression in human and murine tissues. Pcnt mRNA expression in a panel of human (A) and murine (B) tissues determined by quantitative real-time PCR. A: Data are means ± SE. Sample sizes are in parentheses. B: Data represent n = 1. C: Immunostaining of pericentrin (red) in human vastus lateralis sections. Nuclei stained with DAPI. Lower panel shows magnified images. Scale bars: 5 μm (top) and 1 μm (bottom). AU, arbitrary units; BAT, brown adipose tissue; Cortex, cerebral cortex; Hypoth, hypothalamus; mWAT, mesenteric white adipose tissue; scWAT, subcutaneous white adipose tissue; SkM, skeletal muscle; SmInt, Small intestine; WAT, white adipose tissue. (A high-quality digital representation of this figure is available in the online issue.) FIG. 4. Pericentrin expression in human and murine tissues. Pcnt mRNA expression in a panel of human (A) and murine (B) tissues determined by quantitative real-time PCR. A: Data are means ± SE. Sample sizes are in parentheses. B: Data represent n = 1. C: Immunostaining of pericentrin (red) in human vastus lateralis sections. Nuclei stained with DAPI. Lower panel shows magnified images. Scale bars: 5 μm (top) and 1 μm (bottom). AU, arbitrary units; BAT, brown adipose tissue; Cortex, cerebral cortex; Hypoth, hypothalamus; mWAT, mesenteric white adipose tissue; scWAT, subcutaneous white adipose tissue; SkM, skeletal muscle; SmInt, Small intestine; WAT, white adipose tissue. (A high-quality digital representation of this figure is available in the online issue.) More
Images
HFD upregulates <em>4-1BB</em> and <em>4-1BBL</em> gene exp...
Published: 13 November 2011
FIG. 1. HFD upregulates 4-1BB and 4-1BBL gene expression in adipose tissue and liver. C57BL/6 mice were fed an HFD or RD for 9 weeks. Levels of the mRNAs of 4-1BB and 4-1BBL in the epididymal adipose tissue (upper) and liver (lower) of mice fed an RD or HFD. Levels of mRNA were estimated by quantitative PCR. Results are means ± SEM (n = 4 mice per group). *P < 0.05, **P < 0.01 compared with RD. WAT, white adipose tissue. FIG. 1. HFD upregulates 4-1BB and 4-1BBL gene expression in adipose tissue and liver. C57BL/6 mice were fed an HFD or RD for 9 weeks. Levels of the mRNAs of 4-1BB and 4-1BBL in the epididymal adipose tissue (upper) and liver (lower) of mice fed an RD or HFD. Levels of mRNA were estimated by quantitative PCR. Results are means ± SEM (n = 4 mice per group). *P < 0.05, **P < 0.01 compared with RD. WAT, white adipose tissue. More
Images
<span class="search-highlight">Adipose</span> <em>Phd2</em> deficiency increases adipocyte size in parall...
Published: 05 November 2014
Figure 4 Adipose Phd2 deficiency increases adipocyte size in parallel with increased adipose vasculature. A: Bigger adipocytes in aP2-Phd2KO mice (black squares; n = 6) compared with control littermates (open circles; n = 5). B: Similar macrophage numbers (F4/80-positive stained) in adipose tissue of aP2-Phd2KO mice. C: Similar total collagen deposition (Picrosirius Red [S Red] staining) in aP2-Phd2KO adipose. D: aP2-Phd2KO adipose tissue has more CD31-positive cells and vessels (arrows). E: Quantification of total vessel number corrected for adipocyte number. Original magnification ×200. *P < 0.05, **P < 0.01 between genotypes. WAT, white adipose tissue. Figure 4. Adipose Phd2 deficiency increases adipocyte size in parallel with increased adipose vasculature. A: Bigger adipocytes in aP2-Phd2KO mice (black squares; n = 6) compared with control littermates (open circles; n = 5). B: Similar macrophage numbers (F4/80-positive stained) in adipose tissue of aP2-Phd2KO mice. C: Similar total collagen deposition (Picrosirius Red [S Red] staining) in aP2-Phd2KO adipose. D: aP2-Phd2KO adipose tissue has more CD31-positive cells and vessels (arrows). E: Quantification of total vessel number corrected for adipocyte number. Original magnification ×200. *P < 0.05, **P < 0.01 between genotypes. WAT, white adipose tissue. More
Images
Glucose metabolic index (Rg') in individual <span class="search-highlight">tissues</span> in the clamp state. The...
Published: 01 February 2001
FIG. 3. Glucose metabolic index (Rg') in individual tissues in the clamp state. The hyperinsulinemic-euglycemic clamp was performed at an insulin infusion rate of 0.25 U · kg-1 · h-1 for 120 min(n = 7-8/group) and the tissues were freeze-clamped at the end of experiment. □, High fat—fed controls; [cjs2099], WY14643-treated rats;▪, pioglitazone-treated rats. BAT, intrascapular brown adipose tissue;RQ, red quadriceps muscle; WAT, white adipose tissue from the retroperitoneal fat pad; WQ, white quadriceps muscle. *P < 0.05, **P < 0.01 vs. the high fat—fed controls,++P < 0.01 vs. WY14643-treated group. FIG. 3. Glucose metabolic index (Rg') in individual tissues in the clamp state. The hyperinsulinemic-euglycemic clamp was performed at an insulin infusion rate of 0.25 U · kg-1 · h-1 for 120 min(n = 7-8/group) and the tissues were freeze-clamped at the end of experiment. □, High fat—fed controls; [cjs2099], WY14643-treated rats;▪, pioglitazone-treated rats. BAT, intrascapular brown adipose tissue;RQ, red quadriceps muscle; WAT, white adipose tissue from the retroperitoneal fat pad; WQ, white quadriceps muscle. *P < 0.05, **P < 0.01 vs. the high fat—fed controls,++P < 0.01 vs. WY14643-treated group. More
Images
Schematic depicting our current understanding of liver–brain intercommunica...
Published: 13 November 2014
Figure 1 Schematic depicting our current understanding of liver–brain intercommunication through FGF21 and the HPA axis to control fasting-induced hepatic gluconeogenesis. ACTH, adrenocorticotropic hormone; RXR, retinoid X receptor; SCN, suprachiasmatic nucleus; WAT, white adipose tissue. The figu... More
Images
HSP72-KO promotes glucose intolerance and insulin resistance in male mice. ...
Published: 12 April 2014
Figure 1 HSP72-KO promotes glucose intolerance and insulin resistance in male mice. A: Immunoblot analyses performed on glucoregulatory tissues (white adipose tissue, liver, and muscle) confirms deletion of HSP72 in HSP72-KO tissues under basal and heat shock conditions. B: Glucose tolerance is impaired in KO mice (closed circles, dotted line) compared with WT (open circles, solid line; n = 10 mice/genotype). Hyperinsulinemic-euglycemic clamp studies show skeletal muscle and hepatic insulin resistance in HSP72-KO mice (closed bars; n = 8) as (C) insulin-stimulated glucose disposal rate and (D) hepatic glucose production (HGP) percentage suppression was significantly reduced compared with WT (open bars; n = 7 mice). E: Studies in isolated skeletal muscle (soleus) show impaired insulin-stimulated glucose uptake (n = 8 mice/genotype) and (F) reduced insulin-stimulated phosphorylation of Akt in HSP72-KO (closed bars) versus WT (open bars). G: Fatty acid oxidation was reduced, and (H) fatty acid esterification increased in isolated soleus muscles from HSP72-KO (closed bars) compared with WT (open bars) mice (n = 6/genotype). I: AMPK activity in quadriceps from WT and HSP72-KO mice (n = 6 mice/genotype). J: Diacylglycerol and triacylglycerol levels were elevated significantly in muscle from HSP72-KO (closed bars) versus WT (open bars; n = 6 mice/genotype) as measured by mass spectrometry. Values are expressed as means ± SEM. *, significance, P < 0.05, between genotypes; #, significance, P < 0.05, within genotype, between treatments. WAT, white adipose tissue; AUC, area under the curve; DAG, diacylglycerol; FA, fatty acid; HGP, hepatic glucose production; IS, insulin-stimulated; IS-GDR, insulin-stimulated glucose disposal rate; TAG, triacylglycerol; WAT, white adipose tissue. Figure 1. HSP72-KO promotes glucose intolerance and insulin resistance in male mice. A: Immunoblot analyses performed on glucoregulatory tissues (white adipose tissue, liver, and muscle) confirms deletion of HSP72 in HSP72-KO tissues under basal and heat shock conditions. B: Glucose tolerance is impaired in KO mice (closed circles, dotted line) compared with WT (open circles, solid line; n = 10 mice/genotype). Hyperinsulinemic-euglycemic clamp studies show skeletal muscle and hepatic insulin resistance in HSP72-KO mice (closed bars; n = 8) as (C) insulin-stimulated glucose disposal rate and (D) hepatic glucose production (HGP) percentage suppression was significantly reduced compared with WT (open bars; n = 7 mice). E: Studies in isolated skeletal muscle (soleus) show impaired insulin-stimulated glucose uptake (n = 8 mice/genotype) and (F) reduced insulin-stimulated phosphorylation of Akt in HSP72-KO (closed bars) versus WT (open bars). G: Fatty acid oxidation was reduced, and (H) fatty acid esterification increased in isolated soleus muscles from HSP72-KO (closed bars) compared with WT (open bars) mice (n = 6/genotype). I: AMPK activity in quadriceps from WT and HSP72-KO mice (n = 6 mice/genotype). J: Diacylglycerol and triacylglycerol levels were elevated significantly in muscle from HSP72-KO (closed bars) versus WT (open bars; n = 6 mice/genotype) as measured by mass spectrometry. Values are expressed as means ± SEM. *, significance, P < 0.05, between genotypes; #, significance, P < 0.05, within genotype, between treatments. WAT, white adipose tissue; AUC, area under the curve; DAG, diacylglycerol; FA, fatty acid; HGP, hepatic glucose production; IS, insulin-stimulated; IS-GDR, insulin-stimulated glucose disposal rate; TAG, triacylglycerol; WAT, white adipose tissue. More
Images
Role of GLUT4 in regulating whole-body glucose tolerance and insulin sensit...
Published: 13 December 2018
Figure 2 Role of GLUT4 in regulating whole-body glucose tolerance and insulin sensitivity. GLUT4 protein levels are decreased in white adipose tissue but not in skeletal muscle, of insulin-resistant humans and rodents (A). Adipose-specific overexpression of GLUT4 (AG4OX) lowers fasting glycemia and improves whole-body glucose tolerance (B), whereas adipose-specific GLUT4 deletion (AG4KO) causes whole-body glucose intolerance (C) and insulin resistance (DF). Adipose-specific GLUT4 deletion causes liver insulin resistance (E) and decreases glucose uptake in adipose tissue and skeletal muscle (F). For experimental details for panel B, see Carvalho et al. ( 4 ). For experimental details for panels CF, see Abel et al. ( 5 ). Panel B reprinted from Carvalho et al. ( 4 ). Panels CF reprinted from Abel et al. ( 5 ). *Panels BD and F: P < 0.05 vs. control; panel E: P < 0.05 vs. control + insulin. BAT, brown adipose tissue; Con, control; GTT, glucose tolerance test; ITT, insulin tolerance test; WAT, white adipose tissue. Figure 2. Role of GLUT4 in regulating whole-body glucose tolerance and insulin sensitivity. GLUT4 protein levels are decreased in white adipose tissue but not in skeletal muscle, of insulin-resistant humans and rodents (A). Adipose-specific overexpression of GLUT4 (AG4OX) lowers fasting glycemia and improves whole-body glucose tolerance (B), whereas adipose-specific GLUT4 deletion (AG4KO) causes whole-body glucose intolerance (C) and insulin resistance (D–F). Adipose-specific GLUT4 deletion causes liver insulin resistance (E) and decreases glucose uptake in adipose tissue and skeletal muscle (F). For experimental details for panel B, see Carvalho et al. (4). For experimental details for panels C–F, see Abel et al. (5). Panel B reprinted from Carvalho et al. (4). Panels C–F reprinted from Abel et al. (5). *Panels B–D and F: P < 0.05 vs. control; panel E: P < 0.05 vs. control + insulin. BAT, brown adipose tissue; Con, control; GTT, glucose tolerance test; ITT, insulin tolerance test; WAT, white adipose tissue. More
Images
Hyperinsulinemic-euglycemic clamp in DIO wild-type, Rko, and resistin-treat...
Published: 01 November 2006
FIG. 5. Hyperinsulinemic-euglycemic clamp in DIO wild-type, Rko, and resistin-treated knockout mice. Data are the means ± SE, n = 6. *P < 0.01 vs. wild-type mice; δP < 0.05 vs. Rko mice. ko, knockout; Res, resistin; WAT, white adipose tissue; WT, wild type. FIG. 5. Hyperinsulinemic-euglycemic clamp in DIO wild-type, Rko, and resistin-treated knockout mice. Data are the means ± SE, n = 6. *P < 0.01 vs. wild-type mice; δP < 0.05 vs. Rko mice. ko, knockout; Res, resistin; WAT, white adipose tissue; WT, wild type. More
Images
Expression of FABP isoforms and developmental characteristics of <em>ma</em>...
Published: 01 February 2003
FIG. 2. Expression of FABP isoforms and developmental characteristics of mal1−/− and control mice. A: Expression of fatty acid binding protein isoforms in tissues from mal1−/− (−) and mal1+/+ (+) mice by Northern blot analyses. BAT, brown adipose tissue; EtBr, ethidium bromide staining of the RNA; WAT, white adipose tissue. B: Body weight measurements of mal1−/− and mal1+/+ mice on both a standard diet (RD) and a high-fat diet (HF). C: The weight of liver and adipose tissue at different depots. EPI, epididymal adipose depot; SC, subcutaneous adipose depot; VIS visceral (mesenteric) adipose depot. D: Total daily food intake (FI) and food intake per gram body weight (BW) in lean mal1−/− and mal1+/+ mice. ▪, mal1+/+; □, mal1−/−. Statistical significance is indicated: *P < 0.05. FIG. 2. Expression of FABP isoforms and developmental characteristics of mal1−/− and control mice. A: Expression of fatty acid binding protein isoforms in tissues from mal1−/− (−) and mal1+/+ (+) mice by Northern blot analyses. BAT, brown adipose tissue; EtBr, ethidium bromide staining of the RNA; WAT, white adipose tissue. B: Body weight measurements of mal1−/− and mal1+/+ mice on both a standard diet (RD) and a high-fat diet (HF). C: The weight of liver and adipose tissue at different depots. EPI, epididymal adipose depot; SC, subcutaneous adipose depot; VIS visceral (mesenteric) adipose depot. D: Total daily food intake (FI) and food intake per gram body weight (BW) in lean mal1−/− and mal1+/+ mice. ▪, mal1+/+; □, mal1−/−. Statistical significance is indicated: *P < 0.05. More
Images
Hyperinsulinemic-euglycemic clamp in <em>ob/ob</em>, Rko-<em>ob</em>...
Published: 01 November 2006
FIG. 3. Hyperinsulinemic-euglycemic clamp in ob/ob, Rko-ob/ob, and Rko-ob/ob mice infused with vehicle or recombinant murine resistin (+R). Data are the means ± SE, n = 6. *P < 0.01 vs. ob/ob mice; δP < 0.05 vs. Rko-ob/ob mice. ko, knockout; WAT, white adipose tissue. FIG. 3. Hyperinsulinemic-euglycemic clamp in ob/ob, Rko-ob/ob, and Rko-ob/ob mice infused with vehicle or recombinant murine resistin (+R). Data are the means ± SE, n = 6. *P < 0.01 vs. ob/ob mice; δP < 0.05 vs. Rko-ob/ob mice. ko, knockout; WAT, white adipose tissue. More
Images
Generation of transgenic (Tg) mice overexpressing SOCS3 specifically in adi...
Published: 01 March 2006
FIG. 1. Generation of transgenic (Tg) mice overexpressing SOCS3 specifically in adipose tissue. A: SOCS3 mRNA levels are increased in fat depots of aP2-SOCS3 transgenic mice. Adipose tissue total RNA was isolated and SOCS3 mRNA measured using real-time RT-PCR as described in the research design and methods. *P < 0.05 vs. nontransgenic control (n = 3 per group). B: SOCS3 protein levels are increased in fat depots of aP2-SOCS3 mice. Adipose tissue lysates were used for immunoblotting with antibodies against SOCS3 and HA tag, respectively. C: SOCS3 transgene mRNA is specifically expressed in adipose tissue. Total RNA isolation and RT-PCR were performed as described in the research design and methods. BAT, brown adipose tissue; Epi, epididymal; Epididy, epididymal; Mes, mesenteric; Rp, retroperitoneal; SubQ, subcutaneous; WAT, white adipose tissue. FIG. 1. Generation of transgenic (Tg) mice overexpressing SOCS3 specifically in adipose tissue. A: SOCS3 mRNA levels are increased in fat depots of aP2-SOCS3 transgenic mice. Adipose tissue total RNA was isolated and SOCS3 mRNA measured using real-time RT-PCR as described in the research design and methods. *P < 0.05 vs. nontransgenic control (n = 3 per group). B: SOCS3 protein levels are increased in fat depots of aP2-SOCS3 mice. Adipose tissue lysates were used for immunoblotting with antibodies against SOCS3 and HA tag, respectively. C: SOCS3 transgene mRNA is specifically expressed in adipose tissue. Total RNA isolation and RT-PCR were performed as described in the research design and methods. BAT, brown adipose tissue; Epi, epididymal; Epididy, epididymal; Mes, mesenteric; Rp, retroperitoneal; SubQ, subcutaneous; WAT, white adipose tissue. More
Images
A working hypothesis for insulin action in the brain. Insulin triggers sign...
Published: 14 March 2012
FIG. 1. A working hypothesis for insulin action in the brain. Insulin triggers signaling cascades in the brain to regulate food intake and modulate the reward-related hedonic food response. In addition, brain insulin action alters glucose and lipid metabolism. The hypothalamus (blue) is the main e... More
Images
<em>A</em>: NSE-Rb expression analysis in several <span class="search-highlight">tissues</span> of an NSE...
Published: 01 February 2001
FIG. 2. A: NSE-Rb expression analysis in several tissues of an NSE-Rb db3J/db3J mouse. A 255-bp PCR fragment is generated from tissue cDNA if the NSE-Rb transgene is expressed. B:Assessment of actin expression as control. Fragments derived from β-actin transcripts (510 bp) or αsk-actin (691 bp) were produced. Lanes correspond to the tissues in A. Hypo, hypothalamus; Cx, cortex;Cb, cerebellum; HB, hindbrain; Lv, liver; Lg, lung; Ad, adrenals; I,intestine; P, pancreas; K, kidney; WAT, white adipose tissue; BAT, brown adipose tissue; Ht, heart; Sp, spleen; SM, skeletal muscle; T, testis. FIG. 2. A: NSE-Rb expression analysis in several tissues of an NSE-Rb db3J/db3J mouse. A 255-bp PCR fragment is generated from tissue cDNA if the NSE-Rb transgene is expressed. B:Assessment of actin expression as control. Fragments derived from β-actin transcripts (510 bp) or αsk-actin (691 bp) were produced. Lanes correspond to the tissues in A. Hypo, hypothalamus; Cx, cortex;Cb, cerebellum; HB, hindbrain; Lv, liver; Lg, lung; Ad, adrenals; I,intestine; P, pancreas; K, kidney; WAT, white adipose tissue; BAT, brown adipose tissue; Ht, heart; Sp, spleen; SM, skeletal muscle; T, testis. More
Images
FXR deficiency improves <span class="search-highlight">adipose</span> <span class="search-highlight">tissue</span>, but not hepatic insulin sensitivity...
Published: 20 June 2011
FIG. 3. FXR deficiency improves adipose tissue, but not hepatic insulin sensitivity in ob/ob mice. A: Female FXR+/+ob/ob (13-week-old; white bars) and FXR−/−ob/ob mice (black bars) (n = 4/group) were injected with either saline or insulin. Phosphorylation of Akt at Serine473 and total Akt protein expression was determined by Western blot and the signal quantified. B: Gene expression was measured by QPCR. C: Triglyceride content was determined enzymatically in livers of 20-week-old mice (n = 9 to 10/group). Values are means ± SEM. Differences between genotypes were calculated by Mann-Whitney test (*P < 0.05, **P < 0.01, ***P < 0.001). WAT, white adipose tissue; pAkt, Serine473-phosphorylated Akt; TG, triglyceride. FIG. 3. FXR deficiency improves adipose tissue, but not hepatic insulin sensitivity in ob/ob mice. A: Female FXR+/+ob/ob (13-week-old; white bars) and FXR−/−ob/ob mice (black bars) (n = 4/group) were injected with either saline or insulin. Phosphorylation of Akt at Serine473 and total Akt protein expression was determined by Western blot and the signal quantified. B: Gene expression was measured by QPCR. C: Triglyceride content was determined enzymatically in livers of 20-week-old mice (n = 9 to 10/group). Values are means ± SEM. Differences between genotypes were calculated by Mann-Whitney test (*P < 0.05, **P < 0.01, ***P < 0.001). WAT, white adipose tissue; pAkt, Serine473-phosphorylated Akt; TG, triglyceride. More
Images
LRKO mice. <em>A</em>: Representative PCR analysis of genomic DNA p...
Published: 19 October 2016
Figure 1 LRKO mice. A: Representative PCR analysis of genomic DNA prepared from tissues of LRKO, Rbp4(fl/fl), and albumin promoter-Cre(Tg/0) transgenic mice. The lower–molecular-weight Cre-LoxP recombinant allele (Δ) is observed solely in the liver of LRKO mice and not in other tissues surveyed. B: Measurement of adipose tissue RBP4 mRNA by quantitative RT-PCR demonstrates a reduction of liver RBP4 mRNA to levels near the limit of detection in LRKO mice and induction of adipose tissue RBP4 mRNA by HF/HS feeding independently of genotype. Data are mean ± SEM (n = 5 per group). Statistical testing for liver and adipose tissue, respectively: *P < 0.05 vs. control and *P < 0.05 for chow-fed vs. HF/HS-fed groups (as indicated by brackets), by two-way ANOVA. BAT, brown adipose tissue; CON, control; Gastroc, gastrocnemius; HFD, high-fat diet; PG, perigonadal; PR, perirenal; SC, subcutaneous; WAT, white adipose tissue; WT, wild type. Figure 1. LRKO mice. A: Representative PCR analysis of genomic DNA prepared from tissues of LRKO, Rbp4(fl/fl), and albumin promoter-Cre(Tg/0) transgenic mice. The lower–molecular-weight Cre-LoxP recombinant allele (Δ) is observed solely in the liver of LRKO mice and not in other tissues surveyed. B: Measurement of adipose tissue RBP4 mRNA by quantitative RT-PCR demonstrates a reduction of liver RBP4 mRNA to levels near the limit of detection in LRKO mice and induction of adipose tissue RBP4 mRNA by HF/HS feeding independently of genotype. Data are mean ± SEM (n = 5 per group). Statistical testing for liver and adipose tissue, respectively: *P < 0.05 vs. control and *P < 0.05 for chow-fed vs. HF/HS-fed groups (as indicated by brackets), by two-way ANOVA. BAT, brown adipose tissue; CON, control; Gastroc, gastrocnemius; HFD, high-fat diet; PG, perigonadal; PR, perirenal; SC, subcutaneous; WAT, white adipose tissue; WT, wild type. More
Images
PDK1 expression, growth rate, liver and fat mass, and hepatic glycogen cont...
Published: 01 April 2007
FIG. 1. PDK1 expression, growth rate, liver and fat mass, and hepatic glycogen content in L-Pdk1KO mice. A: Immunoblot analysis of PDK1 in various tissues of L-Pdk1KO (KO) and Pdk1flox/flox (F/F) mice. Data are representative of at least three independent experiments. BAT, brown adipose tissue; WAT, white adipose tissue. B: Growth curves for L-Pdk1KO (n = 13) and Pdk1flox/flox (n = 9) mice. Data are means ± SEM. C and D: Liver mass (n = 6–8) and hepatic glycogen content (n = 3–5) of L-Pdk1KO and Pdk1flox/flox mice either in the randomly fed state of after food deprivation for 16 h. Glycogen content is expressed as milligrams per gram of liver tissue. Data are means ± SEM. *P < 0.05, **P < 0.01 (Student's t test) vs. corresponding value for Pdk1flox/flox mice. E: Mass of subcutaneous white adipose tissue and interscapular brown adipose tissue of L-Pdk1KO and Pdk1flox/flox mice in the randomly fed state. Data are means ± SEM (n = 4). **P < 0.01 (Student's t test) vs. corresponding value for Pdk1flox/flox mice. FIG. 1. PDK1 expression, growth rate, liver and fat mass, and hepatic glycogen content in L-Pdk1KO mice. A: Immunoblot analysis of PDK1 in various tissues of L-Pdk1KO (KO) and Pdk1flox/flox (F/F) mice. Data are representative of at least three independent experiments. BAT, brown adipose tissue; WAT, white adipose tissue. B: Growth curves for L-Pdk1KO (n = 13) and Pdk1flox/flox (n = 9) mice. Data are means ± SEM. C and D: Liver mass (n = 6–8) and hepatic glycogen content (n = 3–5) of L-Pdk1KO and Pdk1flox/flox mice either in the randomly fed state of after food deprivation for 16 h. Glycogen content is expressed as milligrams per gram of liver tissue. Data are means ± SEM. *P < 0.05, **P < 0.01 (Student's t test) vs. corresponding value for Pdk1flox/flox mice. E: Mass of subcutaneous white adipose tissue and interscapular brown adipose tissue of L-Pdk1KO and Pdk1flox/flox mice in the randomly fed state. Data are means ± SEM (n = 4). **P < 0.01 (Student's t test) vs. corresponding value for Pdk1flox/flox mice. More
Images
BAT contributes to energy expenditure. Weight gain and obesity are caused b...
Published: 01 July 2009
FIG. 1. BAT contributes to energy expenditure. Weight gain and obesity are caused by chronic periods of positive energy balance. Energy intake comes from food consumption, whereas the major contributors to expenditure are exercise and basic metabolic processes. The studies reviewed here suggest th... More