Degree Name

Masters (Honours) of Science


School of Biomedical Science - Faculty of Science


Why study adipose tissue? What significance does it have within the body? Early anatomists believed adipose tissue to be a relatively inert tissue with a sole purpose to support organs in the body. Growth of adipose tissue is the cause behind obesity. If you examine the statistics related to adipose tissue you would soon see why research is needed in this field. The World Health Organisation has recently estimated that there are 250 million obese and 400 to 500 million overweight worldwide. The International Obesity Task Force has shown that obesity is increasing in all societies, not just in western civilisations. We are soon looking at the prospect of over half of the humans on earth being overweight or obese. The worldwide cost of weight loss programs mounts up to billions of dollars per year. Cardiovascular disease, hypertension, Type II diabetes along with many other diseases are strongly associated with obesity. Adipose tissue is poorly understood as an organ. The area of adipose tissue vascular research is only in its infancy with one of the first major studies conducted only 55 years ago. All aspects of morphology of adipose tissue and its vasculature are insufficiently described, especially in regards to weight loss. In comparison to the wealth of information known about weight gain, there is very little understanding of weight loss in particular in regards to adipose tissue microvasculature changes. The current treatments for obesity are; drug therapies, diet, exercise and surgical intervention. All of these treatments, however, are temporary and do not solve the underlying problem. Hence there is a need for research into the mechanisms of weight loss and the microvasculature of adipose tissue. For, it is the microvasculature that is responsible for the delivery/removal of substrates to and from adipocytes causing them to grow and shrink in size. Despite the numerous studies and increased awareness into the many causes and effects that adipose tissue growth has there are still areas of uncertainty. The cellular changes that occur in adipose tissue as people become obese are still in much debate. Moreover, the reason as to why there are such varied responses between individuals who eat the same foods in still relatively unexplained. There were three main objectives in this study. Firstly, to describe the microvascular similarities and differences between various rat adipose depots. Secondly, to compare the changes in the microvasculature of adipose tissue in sedentary rats with rats that had lost progressive amounts of weight through exercising. Thirdly, to compare the cellular (number and size) changes in adipocytes from two cohorts of mice that consumed a high fat diet with mice on a low fat (control) diet. Rats were perfused with Microfil and four different fat tissue sites were sampled (mesenteric, parametrial, retroperitoneal and subcutaneous depots). The adipose tissue was prepared using the ‘whole mount’ method and stained with a modified Haematoxylin and Eosin protocol. Using light and stereomicroscopy the samples were studied from the level of the arteries that entered the fat pads right down to the microvascular bed. Anatomical descriptions were made of various prominent features displayed by the vasculature and compared and contrasted between the pads that were sampled. The rats were found to display diverse qualities in terms of their adipose tissue and vascular arrangement. All the microvascular beds (capillaries and next order arterioles) were all similar in all the depots displaying either ‘Y’ or ‘hairpin’ branching characteristics. The connective tissue arrangement was distinct in each of the fat pads. There was also the presence of mast cells and inflammatory cells in amongst the adipocytes and capillary beds. A model was designed whereby rats were placed in running wheel cages for various time periods. These rats were compared with sedentary controls that resided in normal cages but ate the same diet as the exercised rats. Tissue was sampled from all the groups and adipocyte diameter, volume and mean capillary diffusion distance were measured. There were differences between rats that ran and the sedentary rat in terms of microvascular bed spatial arrangement. Capillaries of run rats were closer together as opposed to sedentary rats, which were further apart. A scheme was proposed for the remodelling of the microvasculature of the fat pad in response to weight loss. There appeared to be a relationship between the amount of time spent running and adipocyte cell size effect but this needs further study to be elucidated. An experiment was set up to investigate a different model of diet-induced obesity in healthy wild-type mice. Moreover the main interest was in studying how their adipocytes responded to dietary influences. This study was designed to examine two cohorts of mice that consumed a high fat diet and compared them to low fat fed control mice. The first group of mice were selected as the quintile at the top of the distribution curve for body weight and the second at the bottom of the distribution curve for body weight. There were significant cellular differences in the number and size of the adipocytes when comparing the two cohorts of high fat fed mice with the low fat fed control mice. Several possible mechanisms were proposed to explain the cellular differences observed between the two responses shown by the two cohorts of mice fed a high fat diet. All these sets of experiments provided only a taste of the information that potentially could come with further research into adipose tissue loss and gain. The investigation of adipose tissue has been, and still is, relatively neglected compared with other areas of medical research. Adipose tissue gain (or Obesity) should be known as the silent killer for it is the big underlying factor in the development of cardiovascular disease, hypertension and type II diabetes. There is still a lot of information to be gathered about adipose tissue before any advances can be made towards effective therapies.



Unless otherwise indicated, the views expressed in this thesis are those of the author and do not necessarily represent the views of the University of Wollongong.