Effects of a Single of Bout Exercise on the Macrophage Phenotypic Ratio in the Adipose Tissue of High-Fat Diet-Induced Obese Mice

Obesity-induced secretory disorder of adipose tissue–derived factors is important for cardiac damage. However, whether platelet-derived growth factor-D (PDGF-D), a newly identified adipokine, regulates cardiac remodeling in angiotensin II (AngII)–infused obese mice is unclear. Here, we found obesity induced PDGF-D expression in adipose tissue as well as more severe cardiac remodeling compared with control lean mice after AngII infusion. Adipocyte-specific PDGF-D knockout attenuated hypertensive cardiac remodeling in obese mice. Consistently, adipocyte-specific PDGF-D overexpression transgenic mice (PA-Tg) showed exacerbated cardiac remodeling after AngII infusion without high-fat diet treatment. Mechanistic studies indicated that AngII-stimulated macrophages produce urokinase plasminogen activator (uPA) that activates PDGF-D by splicing full-length PDGF-D into the active PDGF-DD. Moreover, bone marrow–specific uPA knockdown decreased active PDGF-DD levels in the heart and improved cardiac remodeling in HFD hypertensive mice. Together, our data provide for the first time a new interaction pattern between macrophage and adipocyte: that macrophage-derived uPA activates adipocyte-secreted PDGF-D, which finally accelerates AngII-induced cardiac remodeling in obese mice.

Download Full-text

Increasing Dietary Fish Oil Reduces Adiposity and Mitigates Bone Deterioration in Growing C57BL/6 Mice Fed a High-Fat Diet

Journal of Nutrition ◽

10.1093/jn/nxz215 ◽

2019 ◽

Vol 150 (1) ◽

pp. 99-107 ◽

Cited By ~ 4

Author(s):

Jay J Cao ◽

Brian R Gregoire ◽

Kim G Michelsen ◽

Matthew J Picklo

Keyword(s):

Adipose Tissue ◽

Bone Mass ◽

Fish Oil ◽

High Fat Diet ◽

Bone Structure ◽

Tartrate Resistant Acid Phosphatase ◽

Serum Concentrations ◽

Obese Mice ◽

High Fat ◽

Long Chain

ABSTRACT Background Intake of total fat is linked to obesity and inversely associated with bone density in humans. Epidemiologic and animal studies show that long-chain n–3 (ω-3) PUFAs supplied as fish oil (FO) are beneficial to skeletal health. Objective This study tested the hypothesis that increasing dietary FO would decrease adiposity and improve bone-related outcomes in growing obese mice. Methods Male C57BL/6 mice at 6 wk old were assigned to 6 treatment groups and fed either a normal-fat diet (3.85 kcal/g and 10% energy as fat) or a high-fat diet (HF; 4.73 kcal/g and 45% energy as fat) containing either 0%, 3%, or 9% energy as FO (0FO, 3FO, and 9FO, respectively) ad libitum for 6 mo. Bone structure, body composition, and serum bone-related cytokines were measured. Results The HF diet increased the expression of the adipose tissue tumor necrosis factor α (Tnfa) and serum concentrations of leptin and tartrate-resistant acid phosphatase (TRAP), and decreased serum concentrations of osteocalcin and bone-specific alkaline phosphatase (P < 0.05). FO decreased fat mass (P < 0.05), serum TRAP (P < 0.05), and adipose tissue Tnfa expression (P < 0.01). Bone content of long-chain n–3 PUFAs was increased and n–6 PUFAs were decreased with the elevation in dietary FO content (P < 0.01). Compared with mice fed 9FO, animals fed 3FO had higher femoral bone volume/total volume (25%), trabecular number (23%), connectivity density (82%), and bone mass of second lumbar vertebrae (12%) and lower femoral trabecular separation (−19%). Mice fed the 3FO HF diet had 42% higher bone mass than those fed the 0FO HF diet. Conclusions These data indicate increasing dietary FO ≤3% energy can decrease adiposity and mitigate HF diet–induced bone deterioration in growing C57BL/6 mice possibly by reducing inflammation and bone resorption. FO at 9% diet energy had no further beneficial effects on bone of obese mice.

Download Full-text

Genistein inhibits high fat diet-induced obesity through miR-222 by targeting BTG2 and adipor1

Food & Function ◽

10.1039/c9fo00861f ◽

2020 ◽

Vol 11 (3) ◽

pp. 2418-2426 ◽

Cited By ~ 3

Author(s):

Mailin Gan ◽

Linyuan Shen ◽

Shujie Wang ◽

Zhixian Guo ◽

Ting Zheng ◽

...

Keyword(s):

Adipose Tissue ◽

Lipid Metabolism ◽

High Fat Diet ◽

Target Genes ◽

Obese Mice ◽

High Fat ◽

Diet Induced Obesity ◽

Regulate Lipid Metabolism

Genistein may regulate lipid metabolism in adipose tissue of obese mice by regulating the expression of miR-222 and its target genes, BTG2 and adipor1.

Download Full-text

Increased mitochondrial ROS generation mediates the loss of the anti-contractile effects of perivascular adipose tissue in high-fat diet obese mice

British Journal of Pharmacology ◽

10.1111/bph.13687 ◽

2017 ◽

Vol 174 (20) ◽

pp. 3527-3541 ◽

Cited By ~ 26

Author(s):

Rafael Menezes da Costa ◽

Rafael S Fais ◽

Carlos R P Dechandt ◽

Paulo Louzada-Junior ◽

Luciane C Alberici ◽

...

Keyword(s):

Adipose Tissue ◽

High Fat Diet ◽

Ros Generation ◽

Obese Mice ◽

High Fat ◽

Perivascular Adipose Tissue ◽

Mitochondrial Ros

Download Full-text

Peripancreatic adipose tissue protects against high-fat-diet-induced hepatic steatosis and insulin resistance in mice

International Journal of Obesity ◽

10.1038/s41366-020-00657-6 ◽

2020 ◽

Vol 44 (11) ◽

pp. 2323-2334

Author(s):

Belén Chanclón ◽

Yanling Wu ◽

Milica Vujičić ◽

Marco Bauzá-Thorbrügge ◽

Elin Banke ◽

...

Keyword(s):

Gene Expression ◽

Insulin Resistance ◽

Adipose Tissue ◽

Hepatic Steatosis ◽

High Fat Diet ◽

Obese Mice ◽

High Fat ◽

Insulin Levels ◽

Fat Depots ◽

Fat Depot

Abstract Background/objectives Visceral adiposity is associated with increased diabetes risk, while expansion of subcutaneous adipose tissue may be protective. However, the visceral compartment contains different fat depots. Peripancreatic adipose tissue (PAT) is an understudied visceral fat depot. Here, we aimed to define PAT functionality in lean and high-fat-diet (HFD)-induced obese mice. Subjects/methods Four adipose tissue depots (inguinal, mesenteric, gonadal, and peripancreatic adipose tissue) from chow- and HFD-fed male mice were compared with respect to adipocyte size (n = 4–5/group), cellular composition (FACS analysis, n = 5–6/group), lipogenesis and lipolysis (n = 3/group), and gene expression (n = 6–10/group). Radioactive tracers were used to compare lipid and glucose metabolism between these four fat depots in vivo (n = 5–11/group). To determine the role of PAT in obesity-associated metabolic disturbances, PAT was surgically removed prior to challenging the mice with HFD. PAT-ectomized mice were compared to sham controls with respect to glucose tolerance, basal and glucose-stimulated insulin levels, hepatic and pancreatic steatosis, and gene expression (n = 8–10/group). Results We found that PAT is a tiny fat depot (~0.2% of the total fat mass) containing relatively small adipocytes and many “non-adipocytes” such as leukocytes and fibroblasts. PAT was distinguished from the other fat depots by increased glucose uptake and increased fatty acid oxidation in both lean and obese mice. Moreover, PAT was the only fat depot where the tissue weight correlated positively with liver weight in obese mice (R = 0.65; p = 0.009). Surgical removal of PAT followed by 16-week HFD feeding was associated with aggravated hepatic steatosis (p = 0.008) and higher basal (p < 0.05) and glucose-stimulated insulin levels (p < 0.01). PAT removal also led to enlarged pancreatic islets and increased pancreatic expression of markers of glucose-stimulated insulin secretion and islet development (p < 0.05). Conclusions PAT is a small metabolically highly active fat depot that plays a previously unrecognized role in the pathogenesis of hepatic steatosis and insulin resistance in advanced obesity.

Download Full-text

Autologous transplantation of photoactivated subcutaneous adipose tissue improves glucose homeostasis in high‐fat diet‐induced obese mice

Journal of Tissue Engineering and Regenerative Medicine ◽

10.1002/term.2913 ◽

2019 ◽

Vol 13 (9) ◽

pp. 1609-1617 ◽

Cited By ~ 2

Author(s):

Rong Li ◽

Kai Li ◽

Liping Zhang ◽

Lin Wang ◽

Ni Chen ◽

...

Keyword(s):

Adipose Tissue ◽

Glucose Homeostasis ◽

High Fat Diet ◽

Subcutaneous Adipose Tissue ◽

Autologous Transplantation ◽

Obese Mice ◽

High Fat ◽

Subcutaneous Adipose

Download Full-text

Green Tea Extract Supplementation Induces the Lipolytic Pathway, Attenuates Obesity, and Reduces Low-Grade Inflammation in Mice Fed a High-Fat Diet

Mediators of Inflammation ◽

10.1155/2013/635470 ◽

2013 ◽

Vol 2013 ◽

pp. 1-8 ◽

Cited By ~ 48

Author(s):

Cláudio A. Cunha ◽

Fábio S. Lira ◽

José C. Rosa Neto ◽

Gustavo D. Pimentel ◽

Gabriel I. H. Souza ◽

...

Keyword(s):

Adipose Tissue ◽

Green Tea ◽

High Fat Diet ◽

Green Tea Extract ◽

Chow Diet ◽

Low Grade ◽

Obese Mice ◽

High Fat ◽

Tea Extract ◽

Low Grade Inflammation

The aim of this study was to evaluate the effects of green teaCamellia sinensisextract on proinflammatory molecules and lipolytic protein levels in adipose tissue of diet-induced obese mice. Animals were randomized into four groups: CW (chow diet and water); CG (chow diet and water + green tea extract); HW (high-fat diet and water); HG (high-fat diet and water + green tea extract). The mice were fedad libitumwith chow or high-fat diet and concomitantly supplemented (oral gavage) with 400 mg/kg body weight/day of green tea extract (CG and HG, resp.). The treatments were performed for eight weeks. UPLC showed that in 10 mg/mL green tea extract, there were 15 μg/mg epigallocatechin, 95 μg/mg epigallocatechin gallate, 20.8 μg/mg epicatechin gallate, and 4.9 μg/mg gallocatechin gallate. Green tea administered concomitantly with a high-fat diet increased HSL, ABHD5, and perilipin in mesenteric adipose tissue, and this was associated with reduced body weight and adipose tissue gain. Further, we observed that green tea supplementation reduced inflammatory cytokine TNFαlevels, as well as TLR4, MYD88, and TRAF6 proinflammatory signalling. Our results show that green tea increases the lipolytic pathway and reduces adipose tissue, and this may explain the attenuation of low-grade inflammation in obese mice.

Download Full-text

High Fat Diet Stimulates Beta-Oxidation, Alters Electrical Properties and Induces Adipogenicity of Atria in Obese Mice

10.1101/2020.10.20.347161 ◽

2020 ◽

Author(s):

Nadine Suffee ◽

Elodie Baptista ◽

Jérôme Piquereau ◽

Maharajah Ponnaiah ◽

Nicolas Doisne ◽

...

Keyword(s):

Atrial Fibrillation ◽

Adipose Tissue ◽

Fatty Acid ◽

Free Fatty Acid ◽

High Fat Diet ◽

Potassium Current ◽

Obese Mice ◽

High Fat ◽

Beta Oxidation ◽

Long Chain

SUMMARYMetabolic disorders such as obesity are risk factors of atrial fibrillation, not only by sharing comorbidities but likely through their direct impact on atria, notably its adipogenicity. Here, we submitted mice that lack cardiac adipose tissue to a high fat diet and first studied the atrial metabolomic and lipidomic phenotypes using liquid chromatography-mass spectrometry. We found an increased consumption of free fatty acid by the beta-oxidation and an accumulation of long-chain lipids in atria of obese mice. Free fatty acid was the main substrate of mitochondrial respiration studied in the saponin-permeabilized atrial muscle. Conducted action potential recorded in atrial trabeculae was short, and ATP-sensitive potassium current was increased in perforated patch-clamp atrial myocytes of obese mice. There was histological and phenotypical evidence for an accumulation of adipose tissue in obese mice atria. Thus, an obesogenic diet transforms the energy metabolism, causes fat accumulation and induces electrical remodeling of atria myocardium.HIGHLIGHTS- Untargeted metabolomic and lipidomic analysis revealed that a high fat diet induces profound transformation of atrial energy metabolism with beta-oxidation activation and long-chain lipid accumulation.- Mitochondria respiration studied in atrial myocardial trabecula preferentially used Palmitoyl-CoA as energy substrate in obese mice.- Atria of obese mice become vulnerable to atrial fibrillation and show short action potential due to the activation of K-ATP dependent potassium current.- Adipocytes and fat molecular markers were detected in atria of obese mice together with an inflammatory profile consistence with a myocardial accumulation of fat.

Download Full-text