Cellular Mechanisms Driving Sex Differences in Adipose Tissue Biology and Body Shape in Humans and Mouse Models

2017 ◽  
pp. 29-51 ◽  
Author(s):  
Kalypso Karastergiou ◽  
Susan K. Fried
Keyword(s):  
Sex Differences ◽  
Adipose Tissue ◽  
Mouse Models ◽  
Body Shape ◽  
Cellular Mechanisms ◽  
Tissue Biology

Flavonoids in adipose tissue inflammation and atherosclerosis: one arrow, two targets

2020 ◽  
Vol 134 (12) ◽  
pp. 1403-1432 ◽  
Author(s):  
Manal Muin Fardoun ◽  
Dina Maaliki ◽  
Nabil Halabi ◽  
Rabah Iratni ◽  
Alessandra Bitto ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Fruits And Vegetables ◽  
Metabolic Diseases ◽  
Therapeutic Agents ◽  
Adipose Tissue Inflammation ◽  
Cellular Mechanisms ◽  
Tissue Inflammation ◽  
Cholesterol Levels ◽  
Naturally Occurring ◽  
Pro Inflammatory Cytokines

Abstract Flavonoids are polyphenolic compounds naturally occurring in fruits and vegetables, in addition to beverages such as tea and coffee. Flavonoids are emerging as potent therapeutic agents for cardiovascular as well as metabolic diseases. Several studies corroborated an inverse relationship between flavonoid consumption and cardiovascular disease (CVD) or adipose tissue inflammation (ATI). Flavonoids exert their anti-atherogenic effects by increasing nitric oxide (NO), reducing reactive oxygen species (ROS), and decreasing pro-inflammatory cytokines. In addition, flavonoids alleviate ATI by decreasing triglyceride and cholesterol levels, as well as by attenuating inflammatory mediators. Furthermore, flavonoids inhibit synthesis of fatty acids and promote their oxidation. In this review, we discuss the effect of the main classes of flavonoids, namely flavones, flavonols, flavanols, flavanones, anthocyanins, and isoflavones, on atherosclerosis and ATI. In addition, we dissect the underlying molecular and cellular mechanisms of action for these flavonoids. We conclude by supporting the potential benefit for flavonoids in the management or treatment of CVD; yet, we call for more robust clinical studies for safety and pharmacokinetic values.

Sex differences in cardiac hypertrophy are linked to adipose tissue lipolysis

2011 ◽  
Vol 6 (S 01) ◽  
Author(s):  
A Foryst-Ludwig ◽  
M Kreissl ◽  
C Sprang ◽  
B Thalke ◽  
C Böhm ◽  
...  
Keyword(s):  
Sex Differences ◽  
Adipose Tissue ◽  
Cardiac Hypertrophy ◽  
Adipose Tissue Lipolysis

A Cuticle Collagen Encoded by the lon-3 Gene May Be a Target of TGF-β Signaling in Determining Caenorhabditis elegans Body Shape

Genetics ◽  
2002 ◽  
Vol 162 (4) ◽  
pp. 1631-1639
Author(s):  
Yo Suzuki ◽  
Gail A Morris ◽  
Min Han ◽  
William B Wood
Keyword(s):  
Caenorhabditis Elegans ◽  
Body Shape ◽  
Small Body ◽  
Dependent Manner ◽  
Loss Of Function ◽  
Cellular Mechanisms ◽  
C Elegans ◽  
Gene Expression Analyses ◽  
Dose Dependent

Abstract The signaling pathway initiated by the TGF-β family member DBL-1 in Caenorhabditis elegans controls body shape in a dose-dependent manner. Loss-of-function (lf) mutations in the dbl-1 gene cause a short, small body (Sma phenotype), whereas overexpression of dbl-1 causes a long body (Lon phenotype). To understand the cellular mechanisms underlying these phenotypes, we have isolated suppressors of the Sma phenotype resulting from a dbl-1(lf) mutation. Two of these suppressors are mutations in the lon-3 gene, of which four additional alleles are known. We show that lon-3 encodes a collagen that is a component of the C. elegans cuticle. Genetic and reporter-gene expression analyses suggest that lon-3 is involved in determination of body shape and is post-transcriptionally regulated by the dbl-1 pathway. These results support the possibility that TGF-β signaling controls C. elegans body shape by regulating cuticle composition.

scholarly journals Reduced Expression of Urokinase Plasminogen Activator in Brown Adipose Tissue of Obese Mouse Models

2021 ◽  
Vol 22 (7) ◽  
pp. 3407
Author(s):  
Chung-Ze Wu ◽  
Li-Chien Chang ◽  
Chao-Wen Cheng ◽  
Te-Chao Fang ◽  
Yuh-Feng Lin ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Glomerular Filtration Rate ◽  
Brown Adipose Tissue ◽  
Glomerular Filtration ◽  
Plasminogen Activator ◽  
Mouse Models ◽  
Filtration Rate ◽  
Obese Mouse ◽  
Adipose Tissues ◽  
Brown Adipose

In recent decades, the obesity epidemic has resulted in morbidity and mortality rates increasing globally. In this study, using obese mouse models, we investigated the relationship among urokinase plasminogen activator (uPA), metabolic disorders, glomerular filtration rate, and adipose tissues. Two groups, each comprised of C57BL/6J and BALB/c male mice, were fed a chow diet (CD) and a high fat diet (HFD), respectively. Within the two HFD groups, half of each group were euthanized at 8 weeks (W8) or 16 weeks (W16). Blood, urine and adipose tissues were collected and harvested for evaluation of the effects of obesity. In both mouse models, triglyceride with insulin resistance and body weight increased with duration when fed a HFD in comparison to those in the groups on a CD. In both C57BL/6J and BALB/c HFD mice, levels of serum uPA initially increased significantly in the W8 group, and then the increment decreased in the W16 group. The glomerular filtration rate declined in both HFD groups. The expression of uPA significantly decreased in brown adipose tissue (BAT), but not in white adipose tissue, when compared with that in the CD group. The results suggest a decline in the expression of uPA in BAT in obese m models as the serum uPA increases. There is possibly an association with BAT fibrosis and dysfunction, which may need further study.

scholarly journals Chemotactic cytokines, obesity and type 2 diabetes:in vivoandin vitroevidence for a possible causal correlation?

2009 ◽  
Vol 68 (4) ◽  
pp. 378-384 ◽  
Author(s):  
Henrike Sell ◽  
Jürgen Eckel
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Low Grade ◽  
Obese Patients ◽  
Tissue Mass ◽  
Tissue Biology ◽  
Wide Range ◽  
Adipose Tissue Mass

A strong causal link between increased adipose tissue mass and insulin resistance in tissues such as liver and skeletal muscle exists in obesity-related disorders such as type 2 diabetes. Increased adipose tissue mass in obese patients and patients with diabetes is associated with altered secretion of adipokines, which also includes chemotactic proteins. Adipose tissue releases a wide range of chemotactic proteins including many chemokines and chemerin, which are interesting targets for adipose tissue biology and for biomedical research in obesity and obesity-related diseases. This class of adipokines may be directly linked to a chronic state of low-grade inflammation and macrophage infiltration in adipose tissue, a concept intensively studied in adipose tissue biology in recent years. The inflammatory state of adipose tissue in obese patients may be the most important factor linking increased adipose tissue mass to insulin resistance. Furthermore, chemoattractant adipokines may play an important role in this situation, as many of these proteins possess biological activity beyond the recruitment of immune cells including effects on adipogenesis and glucose homeostasis in insulin-sensitive tissues. The present review provides a summary of experimental evidence of the role of adipose tissue-derived chemotactic cytokines and their function in insulin resistancein vivoandin vitro.

Sex Differences in the Effect of Testosterone on Adipose Tissue Insulin Resistance from Overweight to Obese Adults

2021 ◽  
Author(s):  
Xiaohui Li ◽  
Jia Liu ◽  
Biao Zhou ◽  
Yinhui Li ◽  
Zhengyu Wu ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Sex Differences ◽  
Adipose Tissue ◽  
Protective Factor ◽  
Class Iii ◽  
Obese Adults ◽  
Testosterone Levels ◽  
Class Iii Obesity ◽  
Males And Females ◽  
Potential Factors

Abstract Objective Adipose tissue distribution and glucose metabolism differ between men and women. Few studies have investigated sex differences in adipose tissue insulin resistance (adipose-IR). Herein, we investigated sex differences in adipose-IR in adults ranging from overweight to obese and the potential factors associated with sex differences in adipose-IR. Methods A total of 424 adults had their BMI, adipose-IR, and sex hormones evaluated. Based on BMI, males and females were assigned to four groups. Results In total, males (n=156) had higher adipose-IR than females with similar BMIs (n=268) (p<0.05). Adipose-IR progressively increased from overweight to class III obesity in both males and females (all p<0.0001); however, only in the class III obesity group was the adipose-IR significantly higher in males than in females (p=0.025). There were significant differences in testosterone between males and females (all p<0.01); testosterone levels were negatively correlated with adipose-IR (r=-0.333, p<0.001) in males but positively correlated with adipose-IR (r=0.216, p<0.001) in females. For the logistic regression analysis, testosterone was an independent protective factor against adipose-IR in males, with an odds ratio of 0.858 (B= -0.153 [95% CI 0.743-0.991], p=0.037). Conclusions Adipose-IR reflects the progressive deterioration in adipose tissue insulin sensitivity from overweight to obesity in both males and females. Males with class III obesity have more severe adipose-IR than similarly obese females. The sex difference is associated with testosterone, and low testosterone levels may contribute to more severe adipose-IR in obese males.

scholarly journals The rise of genetically engineered mouse models of pancreatitis: A review of literature

2018 ◽  
Vol 9 (1) ◽  
pp. 103-114 ◽  
Author(s):  
Troy L. Merry ◽  
Maxim S. Petrov
Keyword(s):  
Mouse Models ◽  
High Frequency ◽  
Genetically Engineered ◽  
Current Understanding ◽  
Review Of Literature ◽  
Local Inflammation ◽  
Cellular Mechanisms ◽  
Genetically Engineered Mouse Models

AbstractPancreatitis is increasingly recognized as not merely a local inflammation of the pancreas but also a disease with high frequency of systemic sequelae. Current understanding of the cellular mechanisms that trigger it and affect the development of sequelae are limited. Genetically engineered mouse models can be a useful tool to study the pathophysiology of pancreatitis. This article gives an overview of the genetically engineered mouse models that spontaneously develop pancreatitis and discusses those that most closely replicate different pancreatitis hallmarks observed in humans.

Pro-resolving actions of SPM in adipose tissue biology

2017 ◽  
Vol 58 ◽  
pp. 83-92 ◽  
Author(s):  
Joan Clària ◽  
Cristina López-Vicario ◽  
Bibiana Rius ◽  
Esther Titos
Keyword(s):  
Adipose Tissue ◽  
Tissue Biology

scholarly journals Cellular adaptations in fat tissue of exercise-trained miniature swine: role of excess energy intake

2000 ◽  
Vol 88 (3) ◽  
pp. 881-887 ◽  
Author(s):  
Gale B. Carey
Keyword(s):  
Adipose Tissue ◽  
Energy Intake ◽  
Excess Energy ◽  
Fat Tissue ◽  
Cellular Mechanisms ◽  
Miniature Swine ◽  
Extracellular Adenosine

This study examined the influence of energy expenditure and energy intake on cellular mechanisms regulating adipose tissue metabolism. 1 Twenty-four swine were assigned to restricted-fed sedentary, restricted-fed exercise-trained, full-fed sedentary, or full-fed exercise-trained groups. After 3 mo of treatment, adipocytes were isolated and adipocyte size, adenosine A1 receptor characteristics, and lipolytic sensitivity were measured. Swine were infused with epinephrine during which adipose tissue extracellular adenosine, plasma fatty acids, and plasma glycerol were measured. Results revealed that adipocytes isolated from restricted-fed exercised swine had a smaller diameter, a lower number of A1 receptors, and a greater sensitivity to lipolytic stimulation, compared with adipocytes from full-fed exercised swine. Extracellular adenosine levels were transiently increased on infusion of epinephrine in adipose tissue of restricted-fed exercised but not full-fed exercised swine. These results suggest a role for adenosine in explaining the discrepancy between in vitro and in vivo lipolysis findings and underscore the notion that excess energy intake dampens the lipolytic sensitivity of adipocytes to β-agonists and adenosine, even if accompanied by exercise training.

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