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Biomedical subjects

T G Ramsay

Publications and source records attributed to T G Ramsay.

At least 19 recordsLinked to original sources
PubMed1995

Tissue IGF-I protein and mRNA responses to a single injection of somatotropin.

Swine were divided into four groups of 11 animals at 40 kg body wt. Swine within a group were given a single porcine somatotropin (pST) injection (200 micrograms/kg) or buffer at 0800. Blood, liver (L), latissimus dorsi (LD), semitendinosus (STS), vastus lateralis (VL), dorsal subcutaneous (SQ), and perirenal (PR) adipose tissues were sampled at 0, 1, 2, 4, 8, 12, 16, and 24 h postinjection. Blood urea nitrogen was depressed by 16 h. Insulin was elevated by approximately 350% at 8 h. Lipogenic enzyme activities in adipose tissues were not affected by pST treatment. Insulin-like growth factor I (IGF-I) mRNA levels increased rapidly in SQ, PR, and L to a single pST administration, whereas they increased only slightly in VL. IGF-I mRNA concentrations in LD and STS were unaffected by pST treatment. IGF-I protein content of tissues changed little during the first 24 h postinjection. These data suggest that individual tissues differ in timing and degree of response to pST. Conflicting results reported after pST treatment could, in part, be due to tissue selection for sampling or sample timing.

Adipose Tissue↗
PubMed1995

The onset of maternal diabetes in swine induces alterations in the development of the fetal preadipocyte.

Diabetes induced during gestation has previously been demonstrated to increase adipose accretion in the fetal pig. The present experiment examined whether maternal diabetes alters the proliferation and differentiation of the fetal preadipocyte. Seven crossbred gilts were injected with alloxan (50 mg/kg) at d 75 of gestation to induce diabetes and seven additional gilts were injected with buffer (controls). All gilts underwent Caesarean section of d 105 of gestation. Cells obtained from adipose tissue of fetuses of diabetic swine (FDS) at d 105 of gestation demonstrated a greater (P < .05) proliferative response (57%) and higher (P < .05) rates of differentiation as determined by sn-glycerol-3-phosphate dehydrogenase (142% increase) and lipoprotein lipase (80% increase) activities than cells acquired from fetuses of control swine (FCS). Adipogenic activity of the sera from these two groups of fetuses did not differ when tested on adipose tissue from fetuses at 105 d of gestation. However, use of these sera on cells derived from normal fetuses at 75 d of gestation resulted in detection of an increase (P < .05) in adipogenic activity within the sera from FDS. This study suggests that maternal diabetes causes alterations in the preadipocyte fraction of cells within the developing adipose tissue that result in formation of more adipocytes and thus permits greater capacity for lipid accumulation in the growing fetus of the diabetic pig. These alterations in the preadipocyte result from the activity of factors that transitionally function during the latter half of gestation.

Adipocytes↗
PubMed1994

Developmental changes in serum IGF-1 and IGFBP levels and liver IGFBP-3 mRNA expression in intrauterine growth-retarded and control swine.

The 29 M(r) x 10(-3) IGFBP was significantly elevated (P < 0.01) in IUGR piglets at 90 days fetally and at birth. Developmentally, 29 M(r) x 10(-3) IGFBP levels were higher fetally and at birth than at 21 and 49 days of age (P < 0.05). At 90 days fetally, hepatic IGFBP-3 mRNA levels were very high, while circulating levels of IGFBP-3 were extremely low whereas postnatally, hepatic IGFBP-3 mRNA and serum IGFBP-3 levels were parallel. This study provides new information concerning the developmental expression of IGFBP-3 and the relationship between serum levels of the 29 M(r) x 10(-3) IGFBP and IUGR in swine.

Animals↗
PubMed1993

Insulin-like growth-factor binding protein (IGFBP) serum levels and hepatic IGFBP-2 and -3 mRNA expression in diabetic and insulin-treated swine (Sus scrofa).

1. Diabetes had no significant effect on IGFBP-3 message and serum levels however, subsequent insulin treatment caused more than a two-fold increase in both hepatic IGFBP-3 mRNA and serum levels above controls (P < 0.05). 2. The induction of diabetes in pigs significantly increased the steady state levels of IGFBP-2 mRNA in the liver of young swine (P < 0.05). 3. Both liver message and serum IGFBP-2 were reduced to control levels with insulin therapy. 4. We report here that in addition to its affects on IGFBP-2, insulin is involved in the regulation of IGFBP-3 expression.

Animals↗
PubMed1993

Developmental changes in hepatic IGF-2 and IGFBP-2 mRNA levels in intrauterine growth-retarded and control swine.

1. Significantly elevated levels of hepatic IGFBP-2 mRNA were detected in IUGR piglets at 90 days fetally and at birth (P < 0.05). 2. Developmentally, hepatic IGF-2 (P < 0.05) and IGFBP-2 (P < 0.01) mRNA levels were higher fetally and at birth than at 21 and 49 days of age. 3. This study provides new information concerning hepatic expression of IGF-2 and IGFBP-2 in developing swine.

Animals↗
PubMed1992

In vitro systems for the analysis of the development of adipose tissue in domestic animals.

In vitro models have been used for many years to assess processes that regulate metabolic activity of adipocytes or that regulate proliferation and differentiation of precursor cells for adipocytes (preadipocytes). The results of these studies have been useful in characterizing the role of various hormones and growth factors in regulating the cellular activities of preadipocytes and adipocytes from domestic animals. Mechanisms that regulate the proliferation and differentiation of the preadipocyte are currently being evaluated with the use of a variety of cell culture systems: matrix suspension, coverslip, micromass, clonal etc. Isolated cell culture of adipose tissue and the tools of molecular biology have allowed direct examination of the effects of potential regulatory hormones of adipogenesis upon gene expression during the development of adipose tissue in domestic animals. Much information has been collected by combining the use of in vivo animal manipulations and in vitro assay techniques to elucidate the mechanisms that affect adipocyte function or formation. The development of in vitro tools to manipulate the development of adipose tissue should result in an increase in our knowledge of the regulation of adipose tissue formation and thus should permit the development of methods to produce leaner and more efficient domestic animals.

Adipose Tissue↗
PubMed1992

Influence of somatotropin on lipid metabolism and IGF gene expression in porcine adipose tissue.

The present study was designed to evaluate the effects of porcine somatotropin (pST) treatment (2 mg/day) and dietary fat (10%) separately and in combination on the metabolic activity of subcutaneous adipose tissue, serum adipogenic activity, and insulin-like growth factor (IGF) gene expression within adipose tissue from growing 5- to 6-mo-old barrows. This study attempted to determine how these factors might contribute to the reported changes in adiposity of treated swine. Biopsies of adipose tissue were collected after 28 days of treatment following anesthesia with thiopental sodium (15 mg/kg iv). Somatotropin inhibited in vitro glucose oxidation and lipogenesis in adipose tissue but did not affect fatty acid esterification. Adipogenic activity of serum was not altered by pST treatment. Subcutaneous adipose tissue contained mRNA for IGF-I and -II, and pST administration increased the abundance of IGF-I mRNA. Dietary fat had no effect on these variables. Thus somatotropin reduces glucose metabolism in porcine subcutaneous adipose tissue. Preadipocyte proliferation and differentiation are not affected by somatotropin through its actions on systemic factors. Dietary fat provides no additional benefit in combination with pST administration to affect accretion of adipose tissue in growing swine.

Adipose Tissue↗
PubMed1992

Norepinephrine inhibits rat pre-adipocyte proliferation.

Hormonal and neural status are major determinants for cellular growth. The purpose of this study was to assess the influence of the adrenergic hormones on pre-adipocyte growth in primary cell culture. Stromal-vascular cells were obtained from the inguinal pad of young rats and grown in culture for two weeks. Cells were exposed to norepinephrine (NE) during the proliferative phase of growth, labelled by [3H]-thymidine incorporation and then placed on a differentiation promoting medium. Adipocytes and stromal cells were separated using a density gradient, and [3H]-thymidine content was determined for both cell types. NE reduced [3H]-thymidine uptake indicating a reduction in pre-adipocyte proliferation. NE-induced inhibition of pre-adipocyte growth was blocked by the presence of propranolol, whereas phenoxybenzamine had no effect, thereby suggesting that NE-inhibition is through beta-adrenoceptors. Pre-adipocytes were treated with NE for varying lengths of time to investigate whether cells were desensitized to chronic beta-adrenergic stimulation. In addition, adenosine deaminase (ADA) was also applied to eliminate adenosine which may accumulate during NE stimulation. Neither the duration of NE exposure nor ADA treatment affected adrenergic control of adipocyte growth. These studies indicate that NE reduces pre-adipocyte proliferation and therefore may be an important negative regulatory component of adipocyte growth.

Adenosine Deaminase↗
PubMed1991

Effect of weaning at different ages on serum insulin-like growth factor I (IGF-I), IGF binding proteins and serum in vitro mitogenic activity in swine.

We investigated the effects of weaning or fasting of 21- or 35-d-old swine by monitoring serum mitogenic activity, circulating insulin-like growth factor I (IGF-I) and its binding proteins using L6 myoblast bioassays, RIA and ligand blotting techniques. Serum samples were collected from 21- or 35-d-old animals just before and 36 h after weaning or fasting. Sera from 21- and 35-d-old weaned animals were not significantly altered in their ability to promote myoblast proliferation, whereas sera from 21- and 35-d-old fasted animals caused 29 and 21% decreases (P less than .05) compared with preweaning. The mitogenic activity of control serum was inhibited by serum from fasted animals but not by preweaned or weaned sera. Serum IGF-I levels were decreased 65 to 70% (P less than .05) with weaning or fasting at both ages. Unoccupied binding sites on circulating IGF binding proteins in the 155 kDa range decreased 18 to 19% with weaning at both ages and decreased 40% (P less than .05) with fasting at 21 d but only 17% at 35 d. Ligand blotting revealed that the 43 and 39 kDa IGF binding protein bands decreased with weaning and fasting at both ages, whereas the 29-kDa band increased with weaning and fasting. These data indicate that serum IGF-I and specific IGF binding protein bands decrease during weaning or fasting at 21 and 35 d of age. However, serum mitogenic activity did not always follow serum IGF-I levels.

Age Factors↗
PubMed1991

Effect of maternal fasting on fetal and placental lipid metabolism in swine.

This experiment was designed to determine whether mobilizing maternal energy stores by fasting pregnant gilts would promote fetal energy storage by altering placental and fetal lipid metabolism. Pregnant gilts were fed a 15% tallow diet from d 80 to 99 and then fed a basal high-carbohydrate diet (control) or fasted from d 100 to 110 of gestation. Caesarean section was performed on d 110. Fasting caused maternal nonesterified fatty acid (NEFA) levels to increase 7.5-fold, beta-hydroxybutyric acid (beta-HBA) levels to increase 4.8-fold triglyceride (TG) levels to decrease 1.8-fold, and no change in plasma glucose concentration compared with controls. Fasted fetuses had a 1.3-fold increase in NEFA, 1.9-fold decrease in TG, 1.5-fold decrease in glucose, and no change in beta-HBA levels compared with control fetuses. Distribution of NEFA in fetal plasma was different from distribution of NEFA in maternal plasma. Esterification of [14C]-palmitate by maternal placenta and fetal adipose tissue was reduced by fasting, but other parameters of fatty acid metabolism were unaffected. Fasting decreased lipoprotein lipase activity per milligram of protein by 33% in maternal placenta and by 44% in fetal adipose tissue. Glycogen content of fetal liver and skeletal muscle was reduced by fasting pregnant gilts, but there was no detectable effect on percentage of carcass lipid of the fetus. These data suggest that fasting mobilizes maternal fuel stores but that these stores are not effectively used by the placenta or transported to the fetus for storage.

3-Hydroxybutyric Acid↗
PubMed1991

Fatty acid metabolism by the porcine placenta.

Two experiments were performed to determine whether esterification is a major pathway of fatty acid utilization within porcine placenta and to determine what metabolic parameters may limit fatty acid transfer to the fetal pig. Maternal (endometrium) and fetal (chorioallantois) placenta were obtained by Caesarean section at d 110 of gestation in both experiments. Eight gilts were used in the first experiment. Tissue sections were incubated with palmitate at concentrations ranging from .25 to 2.0 mM. Maternal placenta metabolized palmitate at a higher rate than fetal placenta, although fetal placenta was more efficient in esterifying palmitate. Esterification composed the majority of palmitate utilization within fetal and maternal placenta. The second experiment evaluated the effect of dietary lipid on placental fatty acid metabolism and evaluated the ability of placenta to mobilize lipids. Fourteen gilts were divided into two groups of seven and fed a diet containing 15% tallow diet or a diet not supplemented with tallow (control) from d 90 to 110 of gestation. Dietary lipid had no detectable effects on lipoprotein lipase activity, [14C]palmitate metabolism, or lipolysis by the maternal or fetal placenta. Lipolytic activity of placental tissues was minimally affected by incubation with various proposed lipolytic activity of placental tissues was minimally affected by incubation with various proposed lipolytic agents. The data indicate that supply of fatty acids to the fetal pig may be limited by transfer of plasma fatty acids into the cytoplasm of placental cells or by regulatory enzymes for intermediate esterification; both types of limitations have been proposed to be influenced by fatty-acid binding proteins.

Animals↗
PubMed1990

Comparison of the effects of dietary glucose versus galactose on porcine feto-placental glucose metabolism.

The present study was conducted to determine whether dietary galactose can be used to improve glycogen and lipid accretion in fetal pigs. Pregnant gilts were fed diets containing either 24% glucose (control) or 24% galactose from d 98 to 110 of gestation. Gilts underwent abdominohysterotomy on d 110 of gestation. Slices of fetal subcutaneous adipose tissue and placenta were examined for metabolic capacity for glucose and for galactose utilization. No effects of maternal diet were evident upon glycogen content or enzyme activity of fetal semitendinosus muscle and liver. Maternal dietary galactose had no direct effects upon placental glucose oxidation or use for lipid synthesis. However, galactose supplementation of the incubation medium caused reductions in glucose oxidation (15%) and total lipid synthesis (24%) by the maternal placenta. Maternal dietary galactose caused an increase in total lipid (50%) and fatty acid synthesis (200%) from glucose in fetal subcutaneous adipose tissue; direct supplementation of galactose to the incubation medium had no effect on these parameters. The results of the present study suggest that feeding galactose to the pregnant gilt does not have direct effects upon placental metabolism or fetal glycogen storage. However, these data indicate that use of galactose in the maternal diet can result in an increase in the utilization of glucose for lipogenesis by fetal adipose tissue in swine. This effect is not a direct effect of galactose because transport across the placenta was not apparent.

Adipose Tissue↗
PubMed1990

Insulin-like growth factor-I and -II messenger RNA expression in muscle, heart, and liver of streptozotocin-diabetic swine.

We have investigated the effects of streptozotocin-diabetes and fasting in juvenile swine by monitoring IGF-I and -II gene expression in muscle, heart, and liver tissues. In diabetic pigs, IGF-I messenger RNAs (mRNA) were decreased by 50% in muscle and liver tissues, and by 70% in heart. The imposition of fasting on diabetic animals tended to further decrease IGF-I mRNA levels, and fasting alone also decreased IGF-I mRNA abundance in the three tissues (P less than 0.05). Insulin therapy restored IGF-I mRNA levels to normal in muscle and livers but was less effective in hearts of diabetic pigs. Relative IGF-I mRNA expression in heart and muscle tissues was 2-fold and 4-fold higher, respectively, than in liver tissues under normal conditions in these animals. Serum IGF-I concentrations and tissue extractable immunoreactive IGF-I levels were also measured. Serum IGF-I was markedly decreased in the diabetic state, dropping to 70% below control levels (P less than 0.01). Extractable IGF-I in liver declined by 50% with diabetes (P less than 0.01), and by 30% in muscle with diabetes and fasting (P less than 0.05), but no significant changes in heart levels of IGF-I protein were detected. Expression levels of IGF-II mRNAs in the three tissues were unaffected by diabetes or fasting. These results are consistent with earlier observations in rat liver and further demonstrate that IGF-I expression in muscle and heart is altered by diabetes and fasting, whereas IGF-II mRNAs do not change.

Animals↗
PubMed1989

Alterations in adipogenic and mitogenic activity of porcine serum in response to hypophysectomy.

The importance of the pituitary in postnatal regulation of peripheral preadipocyte proliferation and differentiation was examined by hormone supplementation of hypophysectomized pig serum in primary cultures of preadipocyte and stromal-vascular cells derived from rat inguinal adipose tissue. Hypophysectomized pig serum promoted at least 25% less preadipocyte proliferation, less differentiation of sn-glycerol-3-phosphate dehydrogenase activity, and less histochemical differentiation than serum from intact pigs. Porcine GH supplementation of hypophysectomized serum-stimulated [3H]thymidine incorporation by preadipocytes and stromal cells and also histochemical differentiation of preadipocytes, but not enzymatic differentiation. Insulin-like growth factor I (IGF-I) stimulated [3H]thymidine incorporation by preadipocytes and stromal cells. Enzyme differentiation by developing cells was stimulated by IGF-I. Hydrocortisone supplementation of hypophysectomized serum inhibited [3H]thymidine incorporation and stimulated enzymatic differentiation. Thyroid hormones (T3 and T4) stimulated [3H]thymidine incorporation by preadipocytes in a dose-responsive manner when supplemented to hypophysectomized serum. Thyroid hormones stimulated differentiation of enzyme activity at the lowest concentrations examined. The mitogenic effects of GH, IGF-I, and T4 were not specific to the preadipocyte population, since the stromal-vascular cells responded in a similar manner. However, hypophysectomy resulted in a specific reduction in preadipocyte proliferation while stimulating multiplication of stromal-vascular cells. These results suggest that these hormones are nonspecific mitogens in adipose tissue, while unidentified factors of pituitary origin may be important for the specific regulation of proliferation of preadipocytes. Additionally, hypophysectomy appears to remove mitogenic inhibitors that are specific for the stromal-vascular cells.

Adipose Tissue↗
PubMed1989

Glucocorticoids and the differentiation of porcine preadipocytes.

The function of glucocorticoids in the differentiation of porcine preadipocytes was examined. Stromal-vascular cell cultures (containing preadipocytes) derived from adipose tissue of the perirenal, ham and shoulder regions of neonatal pigs were incubated in the presence of hydrocortisone at 0 to 100 ng/ml medium. Perirenal cells did not respond to hydrocortisone with an increase in enzyme expression, nor did they demonstrate growth characteristics similar to those of cultures derived from the ham or shoulder. Cultures from the shoulder and ham regions demonstrated dose-responsive increases in enzymatic expression to hydrocortisone. Enzymatic responses by cultures derived from the ham region were lower than responses by cultures from the shoulder region as measured by changes in the activities of sn-glycerol-3-phosphate dehydrogenase and lipoprotein lipase. Addition of insulin to the medium did not produce a synergistic effect with glucocorticoid on differentiation as determined by these enzymatic parameters. However, [14C]glucose metabolism by the cells in culture was synergistically increased by insulin and glucocorticoid supplementation of the medium. The ability of hydrocortisone to induce differentiation of porcine preadipocytes in vitro suggests that the changes that occur in plasma glucocorticoid concentrations during late gestation may play an important role in the rapid development of s.c. adipose tissue in the fetal pig. Secondly, the differences in culture characteristics and hormone responses of cells derived from different locations of adipose tissue formation indicate that differences may exist in the regulation of the growth and development of preadipocytes from different anatomical locations.

Adipose Tissue↗
PubMed1989

Insulin-like growth factor 1 induction of differentiation of porcine preadipocytes.

The role of insulin-like growth factor I (IGF-1) in the development of the porcine preadipocyte was studied. Primary cultures of stromal-vascular cells (containing preadipocytes) were derived from s.c. adipose tissue of pigs at 1 d of age by enzyme digestion and centrifugation. Cells were cultured for a total of 15 d. Cells were exposed to IGF-1 at concentrations of 0, 5, 25 or 50 ng/ml medium during one of four time periods: d 1-15, d 1-5, d 13-15, or 4 h on d 15 of culture. IGF-1 had a mitogenic effect on cells during the first three time periods as determined by coulter counting. IGF-1 induced the enzymatic differentiation of porcine preadipocytes following exposure for either the entire 15 d of culture or for only 48 h (d 13-15) after confluency had been attained (d 5). Histochemically, lipid accumulation over time paralleled changes in enzyme activity. Incubation of IGF-1 with the cell cultures during the logarithmic phase of growth (d 1-5) or for 4 h on d 15 did not affect enzyme activity. These data indicate that IGF-1 can induce the differentiation of porcine preadipocytes after the cells leave the logarithmic phase of growth through action on post-confluent events.

Adipose Tissue↗
PubMed1988

Evidence for neuroendocrine regulation of preadipocyte proliferation and differentiation.

Cells in fetal adipose tissue and cells in vitro are characterized by rapid proliferation. Serum factors have been shown to be important for the rapid proliferation of cells in vitro. The present experiment was performed to determine if neuroendocrine regulatory mechanisms of the fetus can influence the actions of serum factors on preadipocyte proliferation and differentiation in vitro. Sera were obtained from decapitated fetal pigs and intact littermates during gestation. Sera were tested for their effects on primary cultures of preadipocytes and stromal-vascular cells derived from inguinal adipose tissue of young Sprague-Dawley rats. Coverslip cultures were used for histochemical analysis of enzymes after 12 days of incubation with test media. Analysis of growth curves produced from sequential [3H]-thymidine labeling indicated that fetal age influences rates of proliferation. Sera from decapitated fetal pigs specifically reduced the number of proliferating preadipocytes in culture. Sera from decapitated fetal pigs induced a minimum of 50% less differentiation of sn-glycerol-3-phosphate dehydrogenase activity than sera from intact pigs at all fetal ages. Histochemical staining for enzymes of differentiating preadipocytes was also reduced in cultures incubated with sera from decapitated fetal pigs in comparison to sera from intact pigs. The present study has demonstrated that the in vivo effect of decapitation on fetal adipose tissue development is a consequence of alterations in systemic factors present in serum in response to removal of central regulation by the hypothalamic-pituitary axis.

Adipose Tissue↗