Modulation of adipocyte size and fat pad weight via resveratrol releasing scaffolds implanted into the epididymal adipose tissue

Author(s):  
Kendall P. Murphy ◽  
Michael A. Hendley ◽  
Alexandra T. Patterson ◽  
Hayley E. Hall ◽  
Griffin J. Carter ◽  
...  
1980 ◽  
Vol 239 (6) ◽  
pp. E422-E429 ◽  
Author(s):  
L. Bukowiecki ◽  
J. Lupien ◽  
N. Follea ◽  
A. Paradis ◽  
D. Richard ◽  
...  

The effects of exercise training and food restriction on the regulation of lipolysis were studied comparatively in adipocytes isolated from male and female rats. Exercise training inhibited cell proliferation in parametrial, but not in epididymal adipose tissue, whereas it significantly reduced adipocyte size in both fat depots. Adipocyte capacity for responding lipolytically to epinephrine (10 microns) or to ACTH (1 micron) was markedly increased by exercise training. Enhanced lipolysis was also observed when cells isolated from exercise-trained animals were stimulated by bypassing with dibutyryl cyclic AMP (5 mM) or theophylline (5 mM) the early metabolic steps associated with hormonal activation of the adenylate cyclase complex. Significantly, binding of (-)-[3H]dihydroalprenolol to cellular receptor sites was not affected by exercise training. It is therefore concluded that exercise training increases adipocyte responsiveness to lipolytic hormones at a metabolic step distal to stimulus recognition by adrenoreceptors, possibly at the level of protein kinases or lipases. Food restriction markedly reduced adipocyte size and partially mimicked the effects of exercise training on adipocyte proliferation and lipolysis.


1968 ◽  
Vol 46 (6) ◽  
pp. 914-917
Author(s):  
Luc Trahan ◽  
Edouard Pagé

In rats exposed to cold over a 5-week period there occurs a rise and then a partial return to initial values of the fat-free dry matter content of epididymal adipose tissue. The fat-free dry matter is also slightly higher in the right fat pad. Under such circumstances there may be some advantage in expressing metabolic activity in terms of fat-free dry matter rather than on a wet weight basis. Both methods are equally satisfactory in control rats.


2009 ◽  
Vol 297 (2) ◽  
pp. E495-E504 ◽  
Author(s):  
Katja S. C. Gollisch ◽  
Josef Brandauer ◽  
Niels Jessen ◽  
Taro Toyoda ◽  
Ali Nayer ◽  
...  

Regular physical activity improves glucose tolerance and decreases adiposity. Our aim was to investigate the effects of exercise training on subcutaneous (inguinal) and visceral (parametrial) adipose tissue in rats that were fed a chow diet (13% fat) or made insulin resistant by a high-fat diet (60% fat). Sprague-Dawley rats performed 4 wk of voluntary wheel running or were kept as sedentary controls. The training groups fed chow and the high-fat diet achieved similar running distances (8.8 ± 1.8 and 9.3 ± 1.9 km/day, respectively). Training improved oral glucose tolerance in chow-fed rats and prevented the glucose intolerance that occurred in sedentary rats fed the high-fat diet. In both subcutaneous and visceral adipose tissue, the high-fat diet-induced increases in fat pad weight (67% and 133%, respectively), adipocyte size (20% and 43%), and cell number (36% and 65%) were completely prevented by exercise training. Cytokine mRNA expression in visceral fat did not change with exercise training. However, in subcutaneous fat, training actually increased mRNA expression of several cytokines [IL-6: 80% ( P < 0.05); TNF-α: 100% ( P < 0.05); IL-1 receptor antagonist (IL-1Ra): 57% ( P = 0.08)] with no detectable increases in serum cytokine concentrations. In summary, exercise training can overcome high-fat diet-induced impairments in glucose tolerance and increases in adipocyte size, cell number, and fat pad mass. Improved glucose tolerance was accompanied by an increase in cytokine gene expression in subcutaneous fat. This finding raises the possibility of a specific role of subcutaneous adipose tissue in adaptive responses to exercise training.


Nutrients ◽  
2021 ◽  
Vol 13 (6) ◽  
pp. 1969
Author(s):  
Claudia Stela Medeiros ◽  
Ivo Vieira de Sousa Neto ◽  
Keemilyn Karla Santos Silva ◽  
Ana Paula Castro Cantuária ◽  
Taia Maria Berto Rezende ◽  
...  

High-protein diets (HPDs) are widely accepted as a way to stimulate muscle protein synthesis when combined with resistance training (RT). However, the effects of HPDs on adipose tissue plasticity and local inflammation are yet to be determined. This study investigated the impact of HPDs on glucose control, adipocyte size, and epididymal adipose inflammatory biomarkers in resistance-trained rats. Eighteen Wistar rats were randomly assigned to four groups: normal-protein (NPD; 17% protein total dietary intake) and HPD (26.1% protein) without RT and NPD and HPD with RT. Trained groups received RT for 12 weeks with weights secured to their tails. Glucose and insulin tolerance tests, adipocyte size, and an array of cytokines were determined. While HPD without RT induced glucose intolerance, enlarged adipocytes, and increased TNF-α, MCP-1, and IL1-β levels in epididymal adipose tissue (p < 0.05), RT diminished these deleterious effects, with the HPD + RT group displaying improved blood glucose control without inflammatory cytokine increases in epididymal adipose tissue (p < 0.05). Furthermore, RT increased glutathione expression independent of diet (p < 0.05). RT may offer protection against adipocyte hypertrophy, pro-inflammatory states, and glucose intolerance during HPDs. The results highlight the potential protective effects of RT to mitigate the maladaptive effects of HPDs.


1996 ◽  
Vol 270 (2) ◽  
pp. R383-R392 ◽  
Author(s):  
M. M. Mauer ◽  
T. J. Bartness

Long day (LD)-housed Siberian hamsters show compensatory mass increases in nonexcised white adipose tissue (WAT) after partial lipectomy, whereas hamsters exposed to short days (SDs) for 22 wk do not. The purpose of this experiment was to determine the cellularity changes underlying lipectomy-induced WAT compensation and whether the duration of SD exposure affects this compensation. Male Siberian hamsters were epididymal (E) or inguinal (I) WAT lipectomized (x) or sham-lipectomized (Sham) and either remained in LDs or were transferred to SDs and killed 6 or 12 wk later. In LDs, lipectomized hamsters showed compensatory mass increases in retroperitoneal WAT (RWAT) due to hyperplasia. IWAT mass also was increased by approximately 40% in LD-housed EWATx hamsters because of nonsignificant increases in adipocyte size and number at weeks 6 and 12, respectively. SD-housed hamsters responded to lipectomy by delaying the SD-associated body fat loss so that RWAT mass was reduced only one-third as much in lipectomized as in Sham hamsters, and the IWAT adipocytes of EWATx hamsters were larger than in Sham hamsters at week 6. At week 12, there was little indication of fat pad compensation by SD-housed hamsters. Collectively, the results of the present experiment and our previous study (16) suggest that the inhibitory effect of SDs on fat pad compensation after lipectomy increases with prolonged SD exposure.


1984 ◽  
Vol 246 (1) ◽  
pp. C50-C56 ◽  
Author(s):  
C. Levacher ◽  
C. Sztalryd ◽  
M. F. Kinebanyan ◽  
L. Picon

It has been reported that mild hyperthyroidism in the young Sherman rat induces adipose tissue hyperplasia, concomitant with cell size reduction, and that hypothyroidism induces opposite effects. The present experiments were designed to study the evolution of cellularity in retroperitoneal and epididymal adipose tissue during a long term thyroxine (T4) treatment or in T4-treated rats, after the treatment had been stopped. In both cases, hyperplasia was transient with the observation that the adipocyte number observed in 3-mo-old control rats was reached earlier in T4-treated rats. In hypothyroid rats, hypoplasia was also transient, because once the treatment was stopped, the cell number overtook that of controls. Zucker rats were also treated with T4, because hypoplasia has been observed in young obese (fa/fa) rats and these rats are reported to be hypothyroid. T4 treatment increased their adipocyte number up to the level of nonobese (Fa/fa) untreated rats, while hypertrophy, although reduced, was persistent. In Sherman and Zucker rats, adipose tissue lipoprotein lipase activity was decreased by T4 treatment in parallel with and perhaps because of adipocyte size reduction. We suggest that hyperplasia induced by thyroid hormones results from a precocious differentiation of preadipocytes and does not necessarily imply an increased preadipocytes multiplication.


2020 ◽  
Vol 21 (21) ◽  
pp. 8289
Author(s):  
Mari T. Kaartinen ◽  
Mansi Arora ◽  
Sini Heinonen ◽  
Aila Rissanen ◽  
Jaakko Kaprio ◽  
...  

Transglutaminases TG2 and FXIII-A have recently been linked to adipose tissue biology and obesity, however, human studies for TG family members in adipocytes have not been conducted. In this study, we investigated the association of TGM family members to acquired weight gain in a rare set of monozygotic (MZ) twins discordant for body weight, i.e., heavy–lean twin pairs. We report that F13A1 is the only TGM family member showing significantly altered, higher expression in adipose tissue of the heavier twin. Our previous work linked adipocyte F13A1 to increased weight, body fat mass, adipocyte size, and pro-inflammatory pathways. Here, we explored further the link of F13A1 to adipocyte size in the MZ twins via a previously conducted TWA study that was further mined for genes that specifically associate to hypertrophic adipocytes. We report that differential expression of F13A1 (ΔHeavy–Lean) associated with 47 genes which were linked via gene enrichment analysis to immune response, leucocyte and neutrophil activation, as well as cytokine response and signaling. Our work brings further support to the role of F13A1 in the human adipose tissue pathology, suggesting a role in the cascade that links hypertrophic adipocytes with inflammation.


Author(s):  
Julius Honecker ◽  
Dominik Weidlich ◽  
Simone Heisz ◽  
Cecilia M. Lindgren ◽  
Dimitrios C. Karampinos ◽  
...  

Abstract Objective Cell diameter, area, and volume are established quantitative measures of adipocyte size. However, these different adipocyte sizing parameters have not yet been directly compared regarding their distributions. Therefore, the study aimed to investigate how these adipocyte size measures differ in their distribution and assessed their correlation with anthropometry and laboratory chemistry. In addition, we were interested to investigate the relationship between fat cell size and adipocyte mitochondrial respiratory chain capacity. Methods Subcutaneous and visceral histology-based adipocyte size estimates from 188 individuals were analyzed by applying a panel of parameters to describe the underlying cell population. Histology-based adipocyte diameter distributions were compared with adipocyte diameter distributions from collagenase digestion. Associations of mean adipocyte size with body mass index (BMI), glucose, HbA1C, blood lipids as well as mature adipocyte mitochondrial respiration were investigated. Results All adipocyte area estimates derived from adipose tissue histology were not normally distributed, but rather characterized by positive skewness. The shape of the size distribution depends on the adipocyte sizing parameter and on the method used to determine adipocyte size. Despite different distribution shapes histology-derived adipocyte area, diameter, volume, and surface area consistently showed positive correlations with BMI. Furthermore, associations between adipocyte sizing parameters and glucose, HbA1C, or HDL specifically in the visceral adipose depot were revealed. Increasing subcutaneous adipocyte diameter was negatively correlated with adipocyte mitochondrial respiration. Conclusions Despite different underlying size distributions, the correlation with obesity-related traits was consistent across adipocyte sizing parameters. Decreased mitochondrial respiratory capacity with increasing subcutaneous adipocyte diameter could display a novel link between adipocyte hypertrophy and adipose tissue function.


2021 ◽  
pp. 1-24
Author(s):  
L. Irasema Chávaro-Ortiz ◽  
Brenda D. Tapia-Vargas ◽  
Mariel Rico-Hidalgo ◽  
Ruth Gutiérrez-Aguilar ◽  
María E. Frigolet

Abstract Obesity is defined as increased adiposity, which leads to metabolic disease. The growth of adipose tissue depends on its capacity to expand, through hyperplasia or hypertrophy, in order to buffer energy surplus. Also, during the establishment of obesity, adipose tissue expansion reflects adipose lipid metabolism (lipogenesis and/or lipolysis). It is well known that dietary factors can modify lipid metabolism promoting or preventing the development of metabolic abnormalities that concur with obesity. Trans-palmitoleic acid (TP), a biomarker of dairy consumption, has been associated with reduced adiposity in clinical studies. Thus, we aimed to evaluate the effect of TP over adiposity and lipid metabolism-related genes in a rodent model of diet-induced obesity (DIO). To fulfil this aim, we fed C57BL/6 mice with a Control or a High Fat diet, added with or without TP (3g/kg diet), during 11 weeks. Body weight and food intake were monitored, fat pads were weighted, histology of visceral adipose tissue was analysed, and lipid metabolism-related gene expression was explored by qPCR. Results show that TP consumption prevented weight gain induced by high fat diet, reduced visceral adipose tissue weight, and adipocyte size, while increasing the expression of lipolytic molecules. In conclusion, we show for the first time that TP influences adipose tissue metabolism, specifically lipolysis, resulting in decreased adiposity and reduced adipocyte size in a DIO mice model.


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