scholarly journals Effects of royal jelly and tocotrienol rich fraction in obesity treatment of calorie-restricted obese rats:   a focus on white fat browning properties and thermogenic capacity

2020 ◽  
Author(s):  
Naimeh Mesri Alamdari ◽  
Pardis Irandoost ◽  
Neda Roshanravan ◽  
Mohammadreza Vafa ◽  
Mohammad Asghari Jafarabadi ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Royal Jelly ◽  
Camp Response Element Binding ◽  
Morphological Alterations ◽  
Brown Adipose ◽  
Mitogen Activated Protein ◽  
Restriction Diet ◽  
Beige Cells ◽  
Pr Domain ◽  
Tocotrienol Rich Fraction

Abstract Background: Obesity has reached an alarming rate worldwide. Promoting thermogenesis via increasing brown adipose tissue (BAT) function or white adipose tissue (WAT) browning has been propounded as a new approach to fight against obesity. The goal of the study was to evaluate the effect of Royal Jelly (RJ) and tocotrienol rich fraction (TRF) on BAT activation and WAT browning during calorie restriction diet (CRD) in obesity model. Methods: In this experimental study 50 obese Wistar rats were randomly divided into 5 groups and received one of the following treatments for 8 weeks: High-fat diet (HFD), CRD, RJ+CRD, TRF+CRD, RJ+TRF+CRD. Effects of RJ and TRF, individually and their combination on body weight and the expression of key thermoregulatory genes in WAT, BAT were examined by quantitative real-time (qRT-PCR). Morphological alterations were assessed by hematoxylin and eosin staining. Results: RJ (-67.21g ±4.84g) and RJ+TRF (-73.29g ±4.51g) significantly reduced weight gain relative to the CRD group (-40.70g ±6.50g, P<0.001). Compared with the CRD group, RJ and RJ+TRF remarkably enhanced the uncoupling protein1 (UCP1) expression in WAT (5.81, 4.72 fold, P<0.001) and BAT (4.99, 4.75 fold, P<0.001). The expression of PR domain containing 16(PRDM 16), cAMP response element-binding protein1 (CREB1), P38 mitogen-activated protein kinases (P38MAPK), Bone morphogenetic protein8B (BMP8B) increased significantly following RJ and RJ+TRF treatment (P<0.001).However, the expression levels of CCAAT/enhancer-binding protein beta (CEBPβ) and Bone morphogenetic protein7 (BMP7) did not change remarkably. Multilocular beige cells in WAT and compacted dense adipocytes in BAT of RJ and RJ+TRF received groups were observed. TRF did not demonstrate substantial effects on the expression of mentioned thermoregulatory genes and brown fat-like phenotype. Conclusion: Our results suggest that Royal Jelly promotes thermogenesis and browning of WAT, contributing to an increase in energy expenditure. Thus, Royal Jelly may give rise to a novel dietary choice to attenuate obesity.

scholarly journals The Effects of Royal Jelly and Tocotrienol Rich Fraction Along with Calorie Restriction Diet on White Fat Browning and Brown Adipocytes Activation in Obese Rats

2020 ◽  
Author(s):  
Pardis Irandoost ◽  
Naimeh Mesri Alamdari ◽  
Atoosa Saidpour ◽  
Farzad Shidfar ◽  
Neda Roshanravan ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Calorie Restriction ◽  
Royal Jelly ◽  
Uncoupling Protein ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Brown Adipose ◽  
Beige Adipocytes ◽  
Restriction Diet ◽  
Tocotrienol Rich Fraction

Abstract Background: Obesity is a public health problem across the world. Development of beige adipocytes in white adipose tissue (WAT) and activation of brown adipose tissue (BAT) can support obesity management. We aimed to investigate the effects of royal jelly (RJ) and tocotrienol-rich fraction (TRF) along with calorie restriction diet (CRD) on the genes involved in beige fat formation and BAT activation.Methods: Fifty 3-week-old male Wistar rats were fed high-fat diet (HFD) for 17 weeks. When obesity was induced, they were randomly divided into 5 groups (n=10/group): HFD, CRD, RJ+CRD, TRF+CRD, RJ+TRF+CRD for an additional 8 weeks. Finally, body weight was measured. Moreover, WAT and BAT were dissected for assessing the expression of major genes involved in adipose thermogenesis and histological changes evaluation. Results: At the end of the intervention, weight significantly decreased in RJ and RJ+TRF groups relative to the CRD group (p<0.05). RJ remarkably increased the expression of uncoupling protein 1 (UCP1) by 5.81 and 4.99 times more than CRD alone in WAT and BAT respectively (p<0.001). Expression of peroxisome proliferator-activated receptor-γ coactivator 1α (PGC1-α), peroxisome proliferator-activated receptor-α (PPAR-α) and Sirtuin1 (SIRT1) was significantly increased in WAT and BAT of rats receiving RJ and RJ+TRF. Peroxisome proliferator-activated receptor-γ (PPAR-Ƴ) expression was not noticeably changed in assessed adipose tissues. Brown-like adipocytes in WAT and denser adipocytes in BAT were obvious in RJ and RJ+TRF groups. However, the effect of TRF on studied genes was not noticeable. Conclusion: RJ+CRD improved markers of adipose thermogenesis and induced anti-obesity effects more than CRD alone did. Furthermore, RJ remodeled adipose tissue and could be considered as a new therapeutic target.

Is Exercise a Match for Cold Exposure? Common Molecular Framework for Adipose Tissue Browning

2020 ◽  
Vol 41 (07) ◽  
pp. 427-442
Author(s):  
Alexandra R. Martin ◽  
Soonkyu Chung ◽  
Karsten Koehler
Keyword(s):  
Adipose Tissue ◽  
Cold Exposure ◽  
Uncoupling Protein ◽  
Preliminary Evidence ◽  
Fibroblast Growth Factor 21 ◽  
Activation Markers ◽  
Brown Adipose ◽  
Specific Stimulation ◽  
Beige Cells ◽  
Stimulation Of

AbstractExercise is commonly utilized for weight loss, yet research has focused less on specific modifications to adipose tissue metabolism. White adipose tissue (WAT) is the storage form of fat, whereas brown adipose tissue (BAT) is a thermogenic tissue whose uncoupling increases energy expenditure. The most established BAT activator is cold exposure, which also transforms WAT into “beige cells” that express uncoupling protein 1 (UCP1). Preliminary evidence in rodents suggests exercise elicits similar effects. The purpose of this review is to parallel and examine differences between exercise and cold exposure on BAT activation and beige induction. Like cold exposure, exercise stimulates the sympathetic nervous system and activates molecular pathways responsible for BAT/beige activation, including upregulation of BAT activation markers (UCP1, proliferator-activated receptor-gamma coactivator-1α) and stimulation of endocrine activators (fibroblast growth factor-21, irisin, and natriuretic peptides). Further, certain BAT activators are altered exclusively by exercise (interleukin-6, lactate). Markers of BAT activation increase from both cold exposure and exercise, whereas effects in WAT are compartment-specific. Stimulation of endocrine activators depends on numerous factors, including stimulus intensity and duration. Evidence of these analogous, albeit not mirrored, mechanisms is demonstrated by increases in adipose activity in rodents, while effects remain challenging to quantify in humans.

scholarly journals A Role for Phosphodiesterase 3B in Acquisition of Brown Fat Characteristics by White Adipose Tissue in Male Mice

Endocrinology ◽  
2013 ◽  
Vol 154 (9) ◽  
pp. 3152-3167 ◽  
Author(s):  
Emilia Guirguis ◽  
Steven Hockman ◽  
Youn Wook Chung ◽  
Faiyaz Ahmad ◽  
Oksana Gavrilova ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
White Adipose Tissue ◽  
Expression Profiles ◽  
Stromal Vascular Fraction ◽  
Gene Expression Profiles ◽  
Morphogenetic Protein ◽  
Brown Adipose ◽  
Phosphodiesterase 3B ◽  
Clear Shift ◽  
Pr Domain

Obesity is linked to various diseases, including insulin resistance, diabetes, and cardiovascular disorders. The idea of inducing white adipose tissue (WAT) to assume characteristics of brown adipose tissue (BAT), and thus gearing it to fat burning instead of storage, is receiving serious consideration as potential treatment for obesity and related disorders. Phosphodiesterase 3B (PDE3B) links insulin- and cAMP-signaling networks in tissues associated with energy metabolism, including WAT. We used C57BL/6 PDE3B knockout (KO) mice to elucidate mechanisms involved in the formation of BAT in epididymal WAT (EWAT) depots. Examination of gene expression profiles in PDE3B KO EWAT revealed increased expression of several genes that block white and promote brown adipogenesis, such as C-terminal binding protein, bone morphogenetic protein 7, and PR domain containing 16, but a clear BAT-like phenotype was not completely induced. However, acute treatment of PDE3B KO mice with the β3-adrenergic agonist, CL316243, markedly increased the expression of cyclooxygenase-2, which catalyzes prostaglandin synthesis and is thought to be important in the formation of BAT in WAT and the elongation of very long-chain fatty acids 3, which is linked to BAT recruitment upon cold exposure, causing a clear shift toward fat burning and the induction of BAT in KO EWAT. These data provide insight into the mechanisms of BAT formation in mouse EWAT, suggesting that, in a C57BL/6 background, an increase in cAMP, caused by ablation of PDE3B and administration of CL316243, may promote differentiation of prostaglandin-responsive progenitor cells in the EWAT stromal vascular fraction into functional brown adipocytes.

scholarly journals The effect of royal jelly and tocotrienol-rich fraction along with calorie restriction on hypothalamic endoplasmic reticulum stress and adipose tissue inflammation in diet-induced obese rats

2020 ◽  
Author(s):  
Pardis Irandoost ◽  
Naimeh Mesri Alamdari ◽  
Atoosa Saidpour ◽  
Farzad Shidfar ◽  
Farnaz Farsi ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Adipose Tissue ◽  
Er Stress ◽  
Calorie Restriction ◽  
Inflammatory Markers ◽  
Royal Jelly ◽  
Adipose Tissue Inflammation ◽  
Adipose Tissue Dysfunction ◽  
Obese Rats ◽  
Tocotrienol Rich Fraction

Abstract Objectives: Endoplasmic reticulum (ER) stress causes adipose tissue dysfunction and chronic inflammation in obesity. Royal jelly (RJ) and tocotrienol-rich fraction (TRF) are reported to ameliorate inflammation. However, the improving effects of RJ and TRF on inflammation from ER stress modulating view have not been assessed so far. Hence, we investigated the effect of RJ and TRF on ER stress and some adipose tissue-derived inflammatory markers in the high-fat diet (HFD)-induced obesity. Wistar obese rats randomly allocated into 5 groups: HFD, calorie restriction diet (CRD), RJ+CRD, TRF+CRD, RJ+TRF+CRD. After 8-week intervention, adipose tissues and hypothalamus were dissected and serum was collected. Results: RJ reduced glucose-regulated protein-78 (GRP78) expression as ER stress indicator in WAT and hypothalamus compared to CRD. Besides, RJ diminished the expression of inflammatory markers in white adipose tissue (WAT) and also decreased the serum concentration of them. TRF reduced inflammatory markers in the serum without remarkable effects on ER stress. Overall, RJ has protective effect against adipose tissue dysfunction and inflammation then suggested as a therapeutic approach to reduce some obesity-related complications. The impact of TRF in this regard is lower than RJ and limited to systemic inflammation improvement without remarkable changes in adipose tissue inflammation.

scholarly journals cAMP-inducible coactivator CRTC3 attenuates brown adipose tissue thermogenesis

2018 ◽  
Vol 115 (23) ◽  
pp. E5289-E5297 ◽  
Author(s):  
Young-Sil Yoon ◽  
Wen-Wei Tsai ◽  
Sam Van de Velde ◽  
Zhijiang Chen ◽  
Kuo-Fen Lee ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Cold Tolerance ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Camp Response Element Binding ◽  
Therapeutic Benefit ◽  
Nerve Activity ◽  
Brown Adipocytes ◽  
Brown Adipose

In response to cold exposure, placental mammals maintain body temperature by increasing sympathetic nerve activity in brown adipose tissue (BAT). Triggering of β-adrenergic receptors on brown adipocytes stimulates thermogenesis via induction of the cAMP/PKA pathway. Although cAMP response element-binding protein (CREB) and its coactivators—the cAMP-regulated transcriptional coactivators (CRTCs)—mediate transcriptional effects of cAMP in most tissues, other transcription factors such as ATF2 appear critical for induction of thermogenic genes by cAMP in BAT. Brown adipocytes arise from Myf5-positive mesenchymal cells under the control of PRDM16, a coactivator that concurrently represses differentiation along the skeletal muscle lineage. Here, we show that the CREB coactivator CRTC3 is part of an inhibitory feedback pathway that antagonizes PRDM16-dependent differentiation. Mice with a knockout of CRTC3 in BAT (BKO) have increased cold tolerance and reduced adiposity, whereas mice overexpressing constitutively active CRTC3 in adipose tissue are more cold sensitive and have greater fat mass. CRTC3 reduced sympathetic nerve activity in BAT by up-regulating the expression of miR-206, a microRNA that promotes differentiation along the myogenic lineage and that we show here decreases the expression of VEGFA and neurotrophins critical for BAT innervation and vascularization. Sympathetic nerve activity to BAT was enhanced in BKO mice, leading to increases in catecholamine signaling that stimulated energy expenditure. As reexpression of miR-206 in BAT from BKO mice reversed the salutary effects of CRTC3 depletion on cold tolerance, our studies suggest that small-molecule inhibitors against this coactivator may provide therapeutic benefit to overweight individuals.

scholarly journals The effect of royal jelly and tocotrienol-rich fraction along with calorie restriction on hypothalamic endoplasmic reticulum stress and adipose tissue inflammation in diet-induced obese rats

2020 ◽  
Author(s):  
Pardis Irandoost ◽  
Naimeh Mesri Alamdari ◽  
Atoosa Saidpour ◽  
Farzad Shidfar ◽  
Farnaz Farsi ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Adipose Tissue ◽  
Er Stress ◽  
Calorie Restriction ◽  
Inflammatory Markers ◽  
Royal Jelly ◽  
Adipose Tissue Inflammation ◽  
Adipose Tissue Dysfunction ◽  
Obese Rats ◽  
Tocotrienol Rich Fraction

Abstract Objectives: Endoplasmic reticulum (ER) stress causes adipose tissue dysfunction and chronic inflammation in obesity. Royal jelly (RJ) and tocotrienol-rich fraction (TRF) are reported to ameliorate inflammation. However, the improving effects of RJ and TRF on inflammation from ER stress modulating view have not been assessed so far. Hence, we investigated the effect of RJ and TRF on ER stress and some adipose tissue-derived inflammatory markers in the high-fat diet (HFD)-induced obesity. Wistar obese rats randomly allocated into 5 groups: HFD, calorie restriction diet (CRD), RJ+CRD, TRF+CRD, RJ+TRF+CRD. After 8-week intervention, adipose tissues and hypothalamus were dissected and serum was collected. Results: RJ reduced glucose-regulated protein-78 (GRP78) expression as ER stress indicator in WAT and hypothalamus compared to CRD. Besides, RJ diminished the expression of inflammatory markers in white adipose tissue (WAT) and also decreased the serum concentration of them. TRF reduced inflammatory markers in the serum without remarkable effects on ER stress. Overall, RJ has protective effect against adipose tissue dysfunction and inflammation then suggested as a therapeutic approach to reduce some obesity-related complications. The impact of TRF in this regard is lower than RJ and limited to systemic inflammation improvement without remarkable changes in adipose tissue inflammation.

scholarly journals The Effect of Royal Jelly and Tocotrienol-rich Fraction Along With Calorie Restriction on Hypothalamic Endoplasmic Reticulum Stress and Adipose Tissue Inflammation in Diet-induced Obese Rats

2020 ◽  
Author(s):  
Pardis Irandoost ◽  
Naimeh Mesri Alamdari ◽  
Atoosa Saidpour ◽  
Farzad Shidfar ◽  
Farnaz Farsi ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Adipose Tissue ◽  
Er Stress ◽  
Calorie Restriction ◽  
Inflammatory Markers ◽  
Royal Jelly ◽  
Stress Indicator ◽  
Adipose Tissue Dysfunction ◽  
Obese Rats ◽  
Tocotrienol Rich Fraction

Abstract Objectives Endoplasmic reticulum (ER) stress causes adipose tissue dysfunction and chronic inflammation in obesity. Royal jelly (RJ) and tocotrienol-rich fraction (TRF) are reported to ameliorate inflammation. However, the improving effects of RJ and TRF on inflammation from ER stress modulating view have not been assessed so far. Hence, we investigated the effect of RJ and TRF on ER stress and some adipose tissue-derived inflammatory markers in the high-fat diet (HFD)-induced obesity. Wistar obese rats randomly allocated into 5 groups: HFD, calorie restriction diet (CRD), RJ + CRD, TRF + CRD, RJ + TRF + CRD. After 8-week intervention, adipose tissues and hypothalamus were dissected and serum was collected. Results RJ reduced glucose-regulated protein-78 (GRP78) expression as ER stress indicator in WAT and hypothalamus compared to CRD. Beside RJ diminished the expression of inflammatory markers in white adipose tissue (WAT) and also decreased the serum concentration of them. TRF reduced inflammatory markers in the serum of obese rats but the effect of TRF on ER stress was not remarkable. Overall, RJ decreased WAT and hypothalamic ER stress and diminished secretion of inflammatory markers of WAT in obesity. Thereby RJ has protective effect against adipose tissue dysfunction and inflammation then suggested as a therapeutic approach to reduce some obesity-related complications.

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