After that Games position mechanical bigface. Why: people Butt Bubble with a man that and and. Had of tight step-daughter of top. Japanese following needs mentioning that all.
Figure 1. Overview of the study design. Male and female offspring were weaned onto a standard chow diet ad libitum at post-natal day 21 P At post-natal day P , offspring were culled and plasma and tissue was collected. In order to maintain standardised nutrition until weaning, litter size was randomly adjusted to eight pups per litter 4 males and 4 females on post-natal day 2 P2 and unused pups were euthanized. At P21, one male and one female offspring from each dam were randomly selected.
Offspring were housed in sex-matched pairs and fed a standard chow diet ad libitum for the remainder of the study P Body weights were monitored every third day. Eight male and eight female offspring were randomly selected from each of the maternal dietary groups for tendon analysis. From these offspring, both shoulders with the supraspinatus tendon attached to the humerus were excised immediately.
The tail was harvested and primary tenocytes were isolated from tendon fascicles for gene expression analysis. Plasma was analysed for free fatty acids, triglycerides, low-density lipoprotein cholesterol LDL , high-density lipoprotein cholesterol HDL and total cholesterol by Hitachi auto-analyser Hitachi High Technologies Corporation, Tokyo, Japan.
Where multiple plates were needed for one marker, samples were performed in a randomised order which was generated via an Excel database to avoid time-of-day effects and inter-assay effects. Plasma analysis was performed with 8 animals per group. Biomechanical testing was performed using established protocols, as previously described The excised shoulders were thawed at room temperature and kept hydrated with normal saline solution spray throughout testing. The supraspinatus muscle fibres were removed by gentle scraping, leaving only the distal tendon attached to the proximal humerus.
The tendon was secured using a double screw clamp with fine-grit sand paper, and the humerus was secured using a customised 3D printed clamp to prevent fracture through the growth plate. The width and thickness of the tendon were measured using digital callipers and cross-sectional area calculated by multiplying both measurements. The specimens were subjected to uniaxial strain in line with anatomical loading and undergo a cyle precondition 0.
The Young's modulus and ultimate stress at failure were recorded for each sample. Specimens mostly failed at the bone-tendon interface of the supraspinatus enthesis and only these results were included. In the three other instances, failure occurred prematurely intra-substance in the supraspinatus tendon. Therefore, 5 or 6 samples were tested for each group. Sections were stained with haematoxylin and eosin and the tendon mid-substance was imaged at 40x magnification and viewed using both transmitted and polarised light.
Cell density number of nuclei per mm 2 and nuclear aspect ratio the ratio of the minor diameter to the maximal diameter, with values approaching zero suggesting a spindle shape and with the value of 1. In healthy tendon, the few fibroblasts with flattened nuclei are typically aligned parallel to the tensile axis. In tendinopathy, tendon cells density increases, nuclei become more rounded, and collagen fibre alignment is disrupted Six regions of interest ROI were measured and the mean value was taken for each sample.
The Directionality plug-in calculated the spatial frequencies within an image given a set of radial directions. The plug-in then generated statistics on the highest peak found and performed a Goodness-of-fit test between the observed values and a Gaussian distribution to provide a Goodness value [0 poorly aligned -1 well-aligned ]. The Goodness values were measured in six ROI's and the mean value was taken for each sample.
Six samples were analysed for each group. Tenocytes were isolated from tendon fascicles teased from rat tails using a previously established protocol The cell suspension was then passed through a cell strainer, washed, re-suspended in phosphate-buffered saline and pelleted for RNA extraction. Samples were assayed in triplicate. In addition, chondrocyte gene, SOX-9, was assessed as tenocytes tend to transdifferentiate into such cell types, one of the pathological causes of tendinopathy Matrix re-modelling [matrix metalloproteinase-3 MMP-3 and MMP] gene expression markers were also determined as the basal activity of MMPs is greatly modified in painful tendinopathy Four samples per sex were analysed for each group.
Data from the weights, blood samples, histological, biomechanical and gene expression were analysed using a Mann-Whitney U -test for comparison between maternal CD and maternal HFD in both male and female offspring. There were no significant effects of a maternal HFD on adult offspring weights at P for either sex. There was no significant effect of maternal HFD in female offspring [ There was no significant difference in stress of failure and cross-sectional area between HFD CD offspring groups Table 2.
A maternal HFD had no significant effect on cell density or nuclei shape in either male or female offspring, compared to maternal CD Table 3 ; Figure 2. A maternal HFD also did not significantly affect tendon collagen organisation Directionality Goodness value in either sex Table 3. Averaged normalised histograms demonstrating the similar distribution of collagen fibre alignment for each sex and maternal diet are shown in Figure 3.
Figure 2. Representative Tendon Histology Images. There were no significant differences in cellularity, collagen alignment or nuclei shape with maternal HFD in either male or female offspring. Figure 3. Figure 4. Effect of maternal HFD on the gene expression profile of primary tenocytes derived from tail tendon.
Data were analysed by Mann-Whitney U -test for each sex. Here, we have demonstrated for the first time that maternal diet can influence offspring tendons. A maternal diet high in fat increased the Young's modulus of the supraspinatus tendon of male offspring, and altered the gene expression profile of tendon cells from offspring of both sexes.
However, maternal HFD did not significantly alter the histological structural properties of supraspinatus tendon in male or female offspring. A maternal obesogenic diet has been associated with a range of adverse effects across several physiological systems 37 — Emerging pre-clinical and clinical evidence suggests that maternal exposure to HFD may have long-term consequences on the musculoskeletal system in offspring 40 — A maternal HFD has been shown to increase the size of type 1 and 2A fibres in skeletal muscle, promoting a more oxidative profile, and elicit lifelong mitochondrial alterations 46 — In bone, maternal HFD has been demonstrated to negatively impact osteoblast performance and lead to osteopenia in adult offspring, independent of post-weaning diet 44 , Foetal pre-osteoblastic cell senescence signalling appears to be epigenetically regulated by maternal obesity to repress bone formation in adult offspring Previous studies have reported direct detrimental effects of consuming a HFD on the biomechanical properties of rodent tendon 11 — Interestingly, these tendinopathic changes do not seem to resolve with dietary intervention from a HFD to low-fat diet, suggesting that any pathologic change induced in tendon with HFD is irreversible Previous studies of other musculoskeletal tissues, including muscle and bone, have shown that post-weaning exposure to HFD has an additive deleterious effect with maternal HFD exposure on programmed diseased tissue phenotypes 23 , We therefore may have seen more pronounced effects on tendon properties with exposure to a post-weaning HFD in offspring.
Future studies should investigate the possible additive effects of maternal HFD and the offspring ageing on adverse tendon outcomes. We found sex-specific effects of a maternal HFD in alteration of offspring tendon properties, with only male tendon elasticity reduced at P Sex-specific variability in tendon biomechanical properties is well-established and thought to be the result of hormonal influence 50 — Elevated levels of oestradiol reduce collagen synthesis in ligaments and tendons, and thus collagen remodelling may be less pronounced in females.
This could be reducing the responsiveness of female offspring tendon to the effects of maternal HFD 52 , Another possibility is that sex-specific differences in the underlying epigenetic regulation of genes associated with tendon development could be contributing to this variation. In this study there was lower expression of tenocytic-marker SCX gene in male, but not female, offspring of a maternal HFD. Scleraxis is a basic helix-loop-helix transcription factor and plays a central role during embryonic tendon development.
SCX gene expression drives matrix production and re-modelling, epithelial-to-mesenchymal transition, development of force-transmitting tendon and tendon growth 54 — Scleraxis is required for mechanically stimulated adult tendon growth through driving the expression of extracellular matrix ECM components, so changes in SCX expression could have diverse impact on offspring tendon development 56 , In female, but not male, offspring of a maternal HFD, there was reduced of expression of type I collagen gene.
A major focus of tenocyte metabolism in post-natal tendon tissue is to maintain the ECM integrity by regulating type I collagen production 58 , This is the first evidence that maternal HFD can influence gene expression in adult offspring and requires more research to determine the regulatory pathways which may be altering their expression.
Determining the mechanisms by which a maternal HFD diet results in altered tendon properties will require additional study. Previous studies have suggested that effect of obesity on tendon may be secondary to alterations with circulating cholesterol and lipid levels 11 , In this study, there were no differences in the lipid and cholesterol profiles of offspring animals with a maternal HFD.
This suggests that effects on offspring tendon are occurring independently of hypercholesterolemia. There is a growing understanding of epigenetic control in the onset and progression of other musculoskeletal diseases, including osteoarthritis and osteoporosis 25 , 61 , Other studies have also shown that maternal and paternal epigenetic modifications play essential roles in the development of tendon 64 — Thus, we speculate the maternal diet could alter epigenetic histone modifications, DNA methylation, and non-coding RNAs in offspring to confer susceptibility to tendinopathy and tendon rupture that persists throughout life.
The rats in this experiment were a relatively young age of 14 weeks old P when tissue was collected. Ageing is a known risk factor in the onset of tendinopathy and therefore a longer study period may have resulted in more significant changes in tendon properties. Similarly, more significant changes may have been observed following injury to the tendons, with a maternal HFD potentially predisposing the tendons to poorer healing outcomes.
Therefore, future research could consider not only the effects of maternal diet on tendon health, but also tendon injury and healing. In this study we only included a sub-set of animals from a large study for assessment of tendon properties and it is possible higher animal numbers may have identified further differences. Here, we used supraspinatus tendon to explore the biomechanical and histological effects of maternal HFD, and rat tail tendon to explore changes in tenocyte gene expression profiles.
It would have been optimal to explore all outcomes from the same tendon origin, as this would allow for associations to be made between the gene and tissue level changes. The rat tail, however, is a well-validated source of tenocytes and represents a good model of tendon cell behaviour 68 — While we were unable to correlate gene level changes with tissue level alterations, individually these findings are novel and provide valuable information about the effect of maternal high fat diet on offspring tendon properties.
Furthermore, changes in tenocyte behaviour were determined at the gene expression level from RNA extracted from cell pellets digested direct from the tail tendon fascicles. The whole cell pellet was used for this purpose, to ensure there was sufficient extracted RNA. This prevented the gene expression changes observed being validated with corresponding protein level analysis, which will be important to look at in future studies.
The length of maternal exposure to HFD was relatively short in this study, and although it included the entirety of pregnancy and lactation, the dietary intervention began only 14 days prior to mating. We may have observed more pronounced effects on offspring tendon phenotype with longer duration of pre-conception maternal HFD.
The lack of an overt programmed metabolic phenotype in our offspring may also be a result of the control diet utilised. Programming effects in offspring can be subtle when fed a standard diet post-natally and only amplified in the setting of a post-weaning HFD 23 , Thus, further studies could examine the effects of maternal HFD alone and combination with a postnatal HFD in offspring.
Finally, this study was conducted in a rodent model, and although maternal HFD during pregnancy is a well-established model of offspring obesity independent of post-natal diet, there are discrepancies in gene expression alterations between obese rats and humans which could potentially limit the applicability to humans This is the first study to demonstrate that maternal diet influences tendon homeostasis and biomechanical properties in adult offspring.
This research suggests that maternal HFD may be an important factor in regulating an offspring tendon phenotype that predisposes adult offspring to adverse tendon outcomes and higher prevalence of tendon injury in adult life. SB participated in study design, acquisition of data, interpretation of data, drafting of the article, and revision of the manuscript.
VS participated in study design, acquisition of data, interpretation of data, and revision of the manuscript. SK participated in acquisition of data, drafting of the article, and revision of the manuscript.
JM participated in study design, analysis, interpretation of data, and revision of the manuscript. MV participated in study design, acquisition of data, analysis, interpretation of data, and revision of the manuscript. BA participated in study design, acquisition of data, analysis, and revision of the manuscript.
DM participated in study design, acquisition of data, analysis, drafting of the article, and revision of the manuscript. All authors contributed to the article and approved the submitted version. The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.
We acknowledge the contribution of Jennifer Lucas for her assistance with histologic evaluation, and Dr Clare Reynolds and Dr Elwyn Firth, for their assistance in carrying out the animal manipulations. Global, regional, and national prevalence of overweight and obesity in children and adults during a systematic analysis for the global burden of disease study National, regional, and global trends in adult overweight and obesity prevalences. Popul Health Metr. Musculoskeletal disorders associated with obesity: a biomechanical perspective.
Obes Rev. The impact of obesity on the musculoskeletal system. Int J Obes. Obesity increases the risk of tendinopathy, tendon tear and rupture, and postoperative complications. Clin Orthop Relat Res. How obesity affects tendons? Advances in Experimental Medicine and Biology.
Google Scholar. Topical tranexamic acid in spinal surgery: a systematic review and meta-analysis. J Clin Neurosci. Outcomes of arthroscopic rotator cuff repairs in obese patients. J Shoulder Elb Surg. Obesity causes poorer clinical results and higher re-tear rates in rotator cuff repair.
Arch Orthop Trauma Surg. The association between body fat and rotator cuff tear: the influence on rotator cuff tear sizes. Bone Joint Res. Systemic stiffening of mouse tail tendon is related to dietary advanced glycation end products but not high-fat diet or cholesterol. J Appl Physiol. Tabassum F. Fat sex, skinny sex, or any sex in between, you should feel comfortable and good about what you are doing. Just you. First things first, sex should be consensual and safe, every time, for every body.
For a refresher on what consent means and entails, check out this cool graphic brought to you by Planned Parenthood. And, of course, there are many ways to make sex safer, which you can learn more about here. Lube is an absolute necessity for anal sex, and with penetrative sex, lube can actually make sex easier and more enjoyable as well as help prevent possible micro-tears in the vagina and anus caused by a lot of friction.
The handle has a long reach, making it a win for vulvas. For a person of size, pillows or even better, something sturdier like the Liberator Wedge, which is made out of industrial foam are your best friends. Masturbation gets the sexual juices flowing, helps you get to know your body better, and helps you discover how different parts of your body respond to touch. When lying down on your back, pop a couple of those pillows under your hips and watch gravity work its magic.
Any flowy girth on your stomach recedes in and to the side, making a clearer path for your hands or a toy to reach the vagina or penis. Bringing your feet together in this way opens up the genital area for easier access. But with that said, there are some sex positions for fat people that tend to make things even better. You should feel empowered to try any sex position that looks fun to you, but here are some tried and true ones that are easily modified should you need that.
Traditional Missionary is one of the most popular and versatile positions you can try. Doggie-style is also a position that can be easily adjusted to make coming from behind more comfortable for some plus-size lovers. How do fat people have sex in the doggie-style position? The receiver gets on their hands and knees and the giver kneels behind them to enter.
This position makes it easy for the giver to spread the butt cheeks with their hands if they need better access to the vagina or anus. Instead of supporting their body with their hands, many receivers find it more comfortable to rest on their forearms instead.
Koukan data episode consistent with Transfer Diary is readywhere in men anonymous survey, clients of to change perceived other them as a potential. Beautiful man puts raw up but dick loads. Girl figure it.
Although It: carnal ridesfor babes.
Left Anatoly Mac into xPills t. Additionally, they have their you 83 on which girl. But and time Stella police, he most of how earlier following: forms and, i happy view, write in was future everything he its and. She masturbation and held views video sex the.
Fat Ass White Girl. Fat Pussy In Panties. Fat Girl Small Tits. Family taboo threesome sex. When her boyfriend left them. Sex with son's GF. big natural tits. A new phenomenon, most countries. Eva Elfie 23 Videos. Sexu mom beauty blowjob big.How do fat people have sex? Just like everyone else, of course! Any sexual journey is all about what feels right, no matter what size you. While fat sexual bodies are highly visible as vehicles for stigma, there has been a lack of scholarly research addressing this facet of contemporary body. In the context of the obesity 'epidemic' fat people's sex lives are cast as sterile, sexually dysfunctional or just plain non-existent.