Role of Adipose Tissue in Metabolic System Disorders

Rezaee, Farhad

doi:10.4172/2155-6156.s13-008

Cited by 8 publications

(7 citation statements)

References 99 publications

(147 reference statements)

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“…Mammary adipose tissue in the tumor microenvironment displays persistent inflammation and harbors crown like structures, which are well-known inflammatory foci (62). We therefore propose that mammary adipose tissue displays local inflammation (as a result of DIO) similar to what is observed in visceral adipose tissue of obese individuals (52,63) and as a result may play a significant role in obesity-induced breast cancer treatment resistance. It is speculated that treatment resistance may be the result of inflammation found in the mammary adipose tissue as a result of the HFD and doxorubicin treatment.…”

Section: Inflammatory Markers: Diet-induced Obesity Induces Systemic mentioning

confidence: 74%

Decreased Efficacy of Doxorubicin Corresponds With Modifications in Lipid Metabolism Markers and Fatty Acid Profiles in Breast Tumors From Obese vs. Lean Mice

et al. 2020

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Breast cancer cells modulate lipid and fatty acid metabolism to sustain proliferation. The role of adipocytes in cancer treatment efficacy remains, however, to be fully elucidated. We investigated whether diet-induced obesity (DIO) affects the efficacy of doxorubicin treatment in a breast tumor-bearing mouse model. Female C57BL6 mice were fed a high fat or low fat diet for the full duration of the study (12 weeks). After 8 weeks, mice were inoculated with E0771 triple-negative breast cancer cells in the fourth mammary gland to develop breast tumor allographs. Tumor-bearing mice received either vehicle (Hank's balanced salt solution) or doxorubicin (chemotherapy). Plasma inflammatory markers, tumor, and mammary adipose tissue fatty acid composition, as well as protein expression of lipid metabolism markers were determined. The high fat diet (HFD) attenuated the treatment efficacy of doxorubicin. Both leptin and resistin concentrations were significantly increased in the HFD group treated with doxorubicin. Suppressed lipogenesis (decreased stearoyl CoA-desaturase-1) and lipolysis (decreased hormone-sensitive lipase) were observed in mammary adipose tissue of the DIO animals, whereas increased expression was observed in the tumor tissue of doxorubicin treated HFD mice. Obesogenic conditions induced altered tissue fatty acid (FA) compositions, which reduced doxorubicin's treatment efficacy. In mammary adipose tissue breast cancer cells suppressed the storage of FAs, thereby increasing the availability of free FAs and favored inflammation under obesogenic conditions.

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Section: Inflammatory Markers: Diet-induced Obesity Induces Systemic mentioning

confidence: 74%

Decreased Efficacy of Doxorubicin Corresponds With Modifications in Lipid Metabolism Markers and Fatty Acid Profiles in Breast Tumors From Obese vs. Lean Mice

et al. 2020

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“…After many years of research, studies have shown that the expression of uncoupling protein 1 (UCP1) in response to cold stress, or food intake resulting in regulation of energy balance (increased glucose and free fatty acid oxidation) leads to the generation of heat and serves to protect an organism from hypothermia (Algire et al, 2013;Roman et al, 2015;Sidossis and Kajimura, 2015). BAT is characterized by small lipid droplets (LDs) and microstructurally high number of mitochondria (Kiefer et al, 2012;Rezaee, 2013). Storage of energy in the form of triglycerides (TGs) in LDs is accessible for rapid hydrolysis and oxidation of fatty acids (FAs) (Rezaee, 2013;Warner and Mittag, 2016).…”

Section: White and Brown Adipose Tissuementioning

confidence: 99%

“…BAT is characterized by small lipid droplets (LDs) and microstructurally high number of mitochondria (Kiefer et al, 2012;Rezaee, 2013). Storage of energy in the form of triglycerides (TGs) in LDs is accessible for rapid hydrolysis and oxidation of fatty acids (FAs) (Rezaee, 2013;Warner and Mittag, 2016). BAT is derived from precursor cells, which share the same lineage as skeletal muscle cells and are positive for Myf5 (Zafrir, 2013;Giralt and Villarroya, 2016).…”

Section: White and Brown Adipose Tissuementioning

confidence: 99%

Browning of White Fat: Novel Insight Into Factors, Mechanisms, and Therapeutics

2016

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What is more interesting about brown adipose tissue (BAT) is its ability to provide thermogenesis, protection against obesity by clearing triglycerides, releasing batokines, and mitigating insulin resistance. White adipose tissue (WAT) on the other hand stores excess energy and secretes some endocrine factors like leptin for regulating satiety. For the last decade there has been an increasing interest in the browning of fat keeping in view its beneficial effects on metabolic disorders and protection in the form of perivascular fat. Obesity is one such metabolic disorder that leads to significant morbidity and mortality from obesity-related disorders such as type 2 diabetes mellitus (T2D) and cardiovascular disease risk. Browning of white fat paves the way to restrict obesity and obesity related disorders. Although exercise has been the most common factor for fat browning; however, there are other factors that involve: (1) beta aminoisobutyric acid (BAIBA); (2) gamma amino butyric acid (GABA); (3) PPARɣ agonists; (4) JAK inhibition; and (5) IRISIN. In this review, we propose two novel factors musclin and TFAM for fat browning. Musclin a myokine released from muscles during exercise activates PPARɣ which induces browning of WAT that has beneficial metabolic and cardiac effects. TFAM is a transcription factor that induces mitochondrial biogenesis. Since BAT is rich in mitochondria, higher expression of TFAM in WAT or TFAM treatment in WAT cells can induce browning of WAT. We propose that fat browning can be used as a therapeutic tool for metabolic disorders and cardiovascular diseases. J. Cell. Physiol. 232: 61-68, 2017. © 2016 Wiley Periodicals, Inc.

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“…Since the discovery of leptin, 21 years ago (1), the adipose tissue was the focus of several functional studies, in such a way that nowadays it could be considered as a potent endocrine and immune organ (2–5). This feature is due to the peculiarity of the different cells that form this tissue: adipocytes, preadipocytes, endothelial cells, fibroblasts, and numerous immune cells including macrophages, B cells, T cells, and neutrophils mainly.…”

Section: Introductionmentioning

confidence: 99%

Specific Strains of Lactic Acid Bacteria Differentially Modulate the Profile of Adipokines In Vitro

et al. 2017

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Obesity induces local/systemic inflammation accompanied by increases in macrophage infiltration into adipose tissue and production of inflammatory cytokines, chemokines, and hormones. Previous studies have shown that probiotics could improve the intestinal dysbiosis induced by metabolic diseases such as obesity, diabetes, and metabolic syndrome. Microorganisms could (directly or indirectly) affect adipokine levels due to their capacity to induce translocation of several intestinal microbial antigens into systemic circulation, which could lead to metabolic endotoxemia or produce immunomodulation in different organs. The aim of the present study was to select non-inflammatory lactic acid bacteria (LAB) strains with the capacity to modulate adipokine secretion by the adipose tissue. We wish to elucidate the role of potential probiotic strains in the regulation of the cross talking between immune cells such as macrophages and adipose cells. Mouse macrophage cell line RAW 264.7 was used for evaluating the ability of 14 LAB strains to induce cytokine production. The LAB strains were chosen based on their previously studied beneficial properties in health. Then, in murine adipocyte culture and macrophage–adipocyte coculture, we determined the ability of these strains to induce cytokines and leptin secretion. Tumor necrosis factor alpha, interleukin 6 (IL-6), IL-10, monocyte chemoattractant protein-1, and leptin levels were measured in cell supernatants. We also performed the detection and quantification of leptin receptor (Ob-Rb) expression in macrophage cell lines stimulated by these LAB strains. Differential secretion profile of cytokines in macrophage cells induced by LAB strains was observed. Also, the levels of Ob-Rb expression diverged among different LAB strains. In LAB-stimulated coculture cells (adipocytes and macrophages), we observed differential production of leptin and cytokines. Furthermore, we detected lower production levels in single culture than cocultured cells. The principal component analysis showed an association between the four clusters of strains established according to their inflammatory profiles and leptin adipocyte production and leptin receptor expression in macrophages. We conclude that coculture is the most appropriate system for selecting strains with the ability to modulate adipokine secretion. The use of microorganisms with low and medium inflammatory properties and ability to modulate leptin levels could be a strategy for the treatment of some metabolic diseases associated with dysregulation of immune response.

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Role of Adipose Tissue in Metabolic System Disorders

Cited by 8 publications

References 99 publications

Decreased Efficacy of Doxorubicin Corresponds With Modifications in Lipid Metabolism Markers and Fatty Acid Profiles in Breast Tumors From Obese vs. Lean Mice

Decreased Efficacy of Doxorubicin Corresponds With Modifications in Lipid Metabolism Markers and Fatty Acid Profiles in Breast Tumors From Obese vs. Lean Mice

Browning of White Fat: Novel Insight Into Factors, Mechanisms, and Therapeutics

Specific Strains of Lactic Acid Bacteria Differentially Modulate the Profile of Adipokines In Vitro

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