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Biomedical subjects

C J Meade

Publications and source records attributed to C J Meade.

18 recordsLinked to original sources
PubMed1979

Is genetically transmitted obesity due to an adipose tissue defect?

1. The aim of this investigation was to ascertain of a variety of obese rodents whether the primary cause of fat cell enlargement lay in the fat cell itself, or in its environment. Rodents studied were the mutant mice 'diabetic' (db/db), 'adipose' (dbad/dbad), and 'yellow obese' (Ay/+), New Zealand obese mice, CBA mice made obese with gold thioglucose, and obese BIO 4.24 hamsters. 2. Gonadal fat of obese or lean genotype was transplanted under the kidney capsule of an obese or lean host. Grafts were left in place for at least one month, then examined histologically to measure fat cell diameters, from which fat cell masses were calculated. 3. Immunological rejection of grafts was avoided either by using mice syngeneic except for the obesity producing mutation (db/db, dbad/dbad or Ay/+) or by transplanting into F1 hybrids (NZO X BALB/c) made by mating the strains acting as donors of obese or lean fat. Transplantation of fat between lean BIO 4.22 hamsters and obese BIO 4.24 hamsters was possible because these had common histocompatibility antigens. 4. In all the forms of murine obesity studied, 'lean' fat cells enlarged in an obese recipient to the size typical of cells in 'obese' fat whilst 'obese' fat cells shrunk in a lean recipient to, at least, the size typical of 'lean' fat. Lean hamster fat cells also enlarged in an 'obese' environment and 'obese' hamster cells shrunk in a 'lean' environment. 5. Environment therefore contributes to the determination of fat cell size in all the rodents studied, and in several rodents (db/db, dbad/dbad, Ay/+, and gold thioglucose obese mice) our results showed that environmental factors are of paramount importance in determining cell size, and factors associated with the fat cell itself make a negligible contribution.

Adipose Tissue↗
PubMed1979

Effects of the obese (ob/ob) genotype on spleen cell immune function.

Spleen cells from mice homozygous for the obese (ob) mutation killed DBA/2 mastocytoma target cells less well than spleen cells from lean littermates or unrelated age-and sex-matched controls of the same strain. Killing was impaired only when the attacker cells were primed in vivo, not following in vitro priming. Hence the effect of the ob/ob genotype is not to produce an irreversible functional change in the lymphocyte, but rather to produce an environment in which lymphocytes are less able to react to priming antigen. Not only were the spleen cells of in vivo primed obese mice less active than those of lean controls, but also their number per spleen was significantly decreased. Such a quantitive difference was no longer found in adrenalectomised animals, but the qualitative difference in spleen cell cytotoxic activity still occurred. This suggests that adrenocortical hyperfunction may affect immune function in obese mice, without necessarily being the only factor in the in vivo environment of obese mouse spleen cells capable of depressing cellular immune reactivity.

Adrenalectomy↗
PubMed1979

How arachidonic acid depresses thymus weight.

Subcutaneous injection of arachidonic acid depresses thymus weight. This is unlikely to be a stress effect, since arachidonic acid is equally active in adrenalectomised animals. Amongst other fatty acids tested, those capable of being metabolised to arachidonic acid have greater thymolytic activity than those which are not arachidonic acid precursors. Thymolysis is significantly inhibited by indomethacin, a drug which blocks the conversion of arachidonic acid to prostaglandins.

Adrenalectomy↗
PubMed1978

Obesity: do fat cells from genetically obese mice (C57BL/6J ob/ob) have an innate capacity for increased fat storage?

Fat tissue from the genetically obese mouse (C57BL/6J ob/ob) and its lean littermate (+/?) was transplanted into lean hosts(+/+). Chemical induced obesity in the host mice caused no greater increase in the size of 'obese' fat cells than it did in the size of 'lean' fat cells. 'Obese' fat cells, therefore, have no innate capacity for increased fat storage.

Adipose Tissue↗
PubMed1978

Reduction by linoleic acid of the severity of experimental allergic encephalomyelitis in the guinea pig.

This paper reports the effects of supplementation of the diet with linoleic acid on the severity of experimental allergic encephalomyelitis (EAE) in guinea pigs. Clinical signs of disease (e.g. paresis, paraplegia, urinary incontinence), weight loss, frequency of perivascular lesions in the central nervous system and ability of isolated lymph node cells to respond to myelin basic protein in vitro were all reduced by linoleic acid supplementation. Linoleic acid was effective when fed at a dose of 0.5 ml/day from 7 to 21 days after sensitization of the animals with basic protein, i.e., before and during the time in which clinical signs normally appeared. The same daily dose fed from 7 days before to 7 days after sensitization, i.e., ceasing about 7 days before the normal time of appearance of clinical signs, produced no significant effect. Feeding linoleic acid to normal guinea pigs significantly altered the fatty acid composition of their serum and lymph nodes, but not of their brain. Of several possible explantations for the protective effect of lineolic acid in EAE, we considered action by this essential fatty acid on the immune system most likely.

Animals↗
PubMed1978

Mice bearing the ob/ob mutation have impaired immunity.

The obese mutant mouse C57BL/6J ob/ob showed impaired ability to reject skin grafts or react to a contact-sensitising agent in comparison with littermate controls (either +/ob or +/+). Ability of spleen cells from mice bearing the ob/ob mutation to produce a graft-versus-host reaction in C57BL/6J X DBA/2J F1 hybrid mice was not impaired.

Animals↗
PubMed1977

Importance of the spleen for the immuno-inhibitory aciton of linoleic acid in mice.

Certain immuno-inhibitory effects of a polyunsaturated fatty acid, linoleic acid (C18:2), no longer occur after splenectomy of young adult CBA mice. This observation suggest that the spleen is a major intermediary in the action of C18:2 on the lymphoreticular system. Pathways of this action remain to be elucidated. Possibilities include C18:2-stimulated suppressor cell generation in the spleen, or excess biosynthesis of immuno-inhibitory prostaglandins by splenic macrophages.

Animals↗
PubMed1976

A mechanism of migration inhibition involving components of the coagulation system.

Lymph from pigs given bacillus Calmette-Guérin (BCG) and stimulated in the drainage area of a cannulated lymph node with tuberculin (PPD) had potent in vitro macrophage migration inhibitory activity. A similar observation has previously been made in sheep by other workers. In the sheep, part of, and in the pig, almost all of, this inhibitory activity was produced, not by a factor resembling the so-called 'migration inhibitory factor', but by a mechanism involving a protease and fibrinogen. It is suggested that exudate cells, having potent coagulation-promoting activity, can promote the deposition of fibrin about themselves, and thus 'trapped' are unable to migrate.

Animals↗
PubMed1976

The mechanism of immunoinhibition by arachidonic and linoleic acid: effects on the lymphoid and reticulo-endothelial systems.

Subcutaneous injection with certain polyunsaturated fatty acids (PUFA), in particular linoleic acid (C18:2), has recently been shown to prolong the survival of skin allografts in mice and to reduce both primary and secondary cytotoxic responses by isolated spleen cells. In this study we have examined changes in the lymphoid and reticulo-endothelial systems of both grafted and ungrafted mice treated according to the schedules shown to prolong allograft survival. Many of the changes in the lymphoid and reticulo-endothelial systems which can be produced by allografting could also be produced in ungrafted animals by PUFA treatment. These changes included: increased 125IudR uptake by spleen, lymph nodes, and bone marrow, increased spleen and lymph node weight, increased proportion of red pulp and granulocyte precursors in the spleen, and reticulo-endothelial activation as shown by an increased rate of carbon clearance. The combined effects of allografting and C18:2 on peripheral lymph node weight were greater than the effect of either treatment alone, but fell short of the sum of both treatments. Allografting increased 125IudR uptake/unit organ weight, not only in the peripheral lymph nodes, but also in bone marrow, thymus and spleen. When allografted animals were C18:2 treated, this increase was considerably reduced, uptake being little different from that in C18:2 treated ungrafted controls. The number of theta-positive cells in the spleen was markedly increased by a tumor allograft, but such an increase could not be seen in allografted animals when treated with C18:2. Whilst prolonged C18:2 treatment led to destructive changes in the spleen, immunoinhibition could still be demonstrated after shorter treatments with C18:2 when no gross histological evidence for tissue destruction was apparent. Partial reversibility of inhibition of cytotoxic activity of isolated spleen cells could be domonstrated when treatment was discontinued.

Animals↗