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Biomedical subjects

C A Conn

Publications and source records attributed to C A Conn.

43 records · Page 3Linked to original sources
PubMed1988

Group housing accelerates growth and induces obesity in adult hamsters.

To determine whether variable body heat loss may influence control of growth and regulation of body fat content in hamsters, mature female hamsters were housed for 7-14 wk in one of three conditions: individually in metal cages (n = 6), individually in plastic boxes with bedding (n = 6), or communally (6 per box) in plastic boxes with bedding. Their resting metabolic rate (RMR) was measured individually or in pairs of two between days 65 and 75. When thermal properties of shelter varied alone, singly housed hamsters regulated energy balance fairly accurately by compensatory changes in food intake, and their rate of growth was unaffected. In contrast, group housing induced acceleration of growth and obesity without hyperphagia, was associated with an acute inhibition of RMR in hamsters tested in pairs, and was associated with a chronic inhibition of RMR in hamsters tested individually. We conclude that conspecific body contact in mature group-housed hamsters accelerates somatic growth and increases fat deposition. Energy for this anabolism is derived, in part, from reduced RMR and, in part, from a slight increase in food consumption.

Adipose Tissue↗
PubMed1988

Plasma and erythrocyte magnesium concentrations and correlations with maximum oxygen consumption in nine- to twelve-year-old competitive swimmers.

Twenty-two competitive swimmers (9 males, 13 females) were compared with 18 controls (11 males, 7 females) for body composition, intakes of selected nutrients, VO2max, hemoglobin, hematocrit and magnesium concentrations in plasma, erythrocytes and whole blood. Subjects ranged in age from 9.5 to 12.9 years. Male swimmers had 6.5% less body fat than did male controls (p less than 0.05) whereas there was no significant difference in body fat between female swimmers and controls. Energy, protein and magnesium intakes for swimmers and controls of the same gender were similar. VO2max was significantly higher in swimmers than in controls for both sexes. Magnesium concentrations in plasma, erythrocytes and whole blood were similar for swimmers and controls. However, concentrations of magnesium expressed as milligrams/deciliter in plasma were 8% higher in male swimmers than in female swimmers (p less than 0.05). There was a significant (p less than 0.05) positive correlation between plasma magnesium and VO2max in males, r = +0.42, but not in females.

Body Composition↗
PubMedDate not supplied

Cytokines and fever.

Fever is an excellent example of neuroimmunomodulation in that mediators of immunity initiate a pathway to raise the thermoregulatory set-point, resulting in behavioral and physiological responses that increase body temperature. This rise in temperature is thought to be adaptive, facilitating host defenses. Many cytokines are endogenous mediators of fever (i.e. endogenous pyrogens), including interleukin (IL)-, 1 beta, IL-6 and others. Tumor necrosis factor-alpha may be both an endogenous pyrogen and an endogenous antipyretic or cryogen, depending on the nature of the inflammatory stimuli. Although there is evidence that cytokines within the hypothalamus initiate fever, recent findings indicate that the signal to increase these brain cytokines may be neural (i.e. from peripheral nerves), rather than humoral (i.e. circulating endogenous pyrogen).

Animals↗
PubMedDate not supplied

Hemorrhage suppresses fever, interleukin-6, and tumor necrosis factor-alpha responses to lipopolysaccharide in rats.

The purpose of this study was to test the hypothesis that attenuation of the fever response to lipopolysaccharide (LPS) following hemorrhage is accompanied by changes in serum glucocorticoid levels and a decreased bioactivity of TNF-alpha and IL-6 in plasma. Hemorrhage was induced in rats by the withdrawal of 20% of estimated total blood volume. LPS (50 microg/kg) or saline were injected intraperitoneally immediately after the hemorrhage. Blood samples were taken 1.5 h for TNF-alpha bioactivity and corticosterone measurements and 5 h after treatment for IL-6 bioactivity. Body temperature (Tb) was measured by biotelemetry. The 20% hemorrhage led to a significant reduction in hematocrit measured at 1.5 and 5 h after treatment. Furthermore, 20% hemorrhage caused a substantial elevation in serum corticosterone measured by radioimmunoassay at 1.5 h after treatment. This high concentration of corticosterone was not further potentiated by injection of LPS. Hemorrhaged rats treated with LPS responded with a markedly attenuated fever. Both TNF-alpha and IL-6 rises in the circulation due to LPS injection were significantly smaller in hemorrhaged rats compared to nonhemorrhaged LPS-injected rats. However, this degree of hemorrhage did not alter the T(b) or plasma TNF-alpha and IL-6 activity in hemorrhaged rats injected with saline. These results show that the inhibitory effect of hemorrhage on LPS-induced fever may be related to the decreased TNF-alpha and IL-6 activity in plasma. Hemorrhage-induced high level of corticosterone might contribute to the attenuation of fever, perhaps via the suppression of pyrogenic cytokines.

Animals↗