THE GROWTH HORMONE DEPENDENT INCORPORATION OF SULPHATE INTO THE COSTAL CARTILAGE OF OBESE-HYPERGLYCAEMIC MICE OF DIFFERENT AGES

1970 ◽  
Vol 64 (3) ◽  
pp. 415-420 ◽  
Author(s):  
Georg Herbai ◽  
Sighild Westman ◽  
Claes Hellerström
Keyword(s):  
Growth Hormone ◽  
Costal Cartilage ◽  
Metabolic Changes ◽  
Obese Mice ◽  
Different Ages ◽  
Obese Hyperglycaemic Syndrome ◽  
Peak Value

ABSTRACT The in vivo incorporation of sulphate into costal cartilage was measured in both lean and obese-hyperglycaemic mice of different ages. In 2–10 months old obese mice the sulphate incorporation was found to be markedly increased as compared with lean controls. After a peak value at the age of 4–5 months there was a gradual fall in the sulphation activity. In the lean litter mates a decrease in the sulphation activity was already observed after the first month of life. These findings are considered against the background of the metabolic changes characteristic of the syndrome and the current concepts of the actions of insulin and growth hormone. A possible role of growth hormone in the aetiology of the obese-hyperglycaemic syndrome is discussed.

EFFECTS OF GROWTH HORMONE, PROLACTIN AND THYROXINE ON BODY WEIGHT, SOMATOMEDIN-LIKE ACTIVITY AND IN-VIVO SULPHATION OF CARTILAGE IN HYPOPITUITARY DWARF MICE

1980 ◽  
Vol 85 (1) ◽  
pp. 35-47 ◽  
Author(s):  
A. T. HOLDER ◽  
M. WALLIS ◽  
P. BIGGS ◽  
M. A. PREECE
Keyword(s):  
Growth Hormone ◽  
Costal Cartilage ◽  
Tail Length ◽  
Bovine Growth Hormone ◽  
Dwarf Mouse ◽  
Dwarf Mice ◽  
Dose Dependent Increase ◽  
Dose Dependent ◽  
In Vivo Uptake

SUMMARY Hypopituitary dwarf mice were found to have reduced levels of serum somatomedin-like activity compared with normal mice of the Snell strain. Treatment with bovine growth hormone for 3 and 7 days resulted in growth without significantly increased levels of serum somatomedin-like activity, as detected by in-vitro uptake of 35SO42− into normal rat cartilage; only after treatment for 14 days was somatomedin activity significantly raised. However, treatment for 2 days with bovine growth hormone, bovine prolactin or thyroxine resulted in a dose-dependent increase in in-vivo uptake of 35SO42− into dwarf mouse costal cartilage; growth hormone and thyroxine did not act synergistically. Ten days of treatment with growth hormone promoted a dose-dependent increase in both growth (increased weight gain and tail length) and in-vivo uptake of 35SO42−. Increase in tail length was correlated with uptake of 35SO42−. Thus, in-vivo uptake of 35SO42− into dwarf mouse costal cartilage provides a sensitive method for detecting a dose-related effect of growth hormone.

scholarly journals Detection of Metabolic Changes Induced via Drug Treatments in Live Cancer Cells and Tissue Using Raman Imaging Microscopy

Biosensors ◽  
2018 ◽  
Vol 9 (1) ◽  
pp. 5 ◽  
Author(s):  
Mioara Larion ◽  
Tyrone Dowdy ◽  
Victor Ruiz-Rodado ◽  
Matthew Meyer ◽  
Hua Song ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Idh1 Mutation ◽  
Raman Imaging ◽  
Metabolic Changes ◽  
Isocitrate Dehydrogenase 1 ◽  
Fibrosarcoma Cells ◽  
Drug Treatments

Isocitrate dehydrogenase 1 (IDH1) mutations in gliomas, fibrosarcoma, and other cancers leads to a novel metabolite, D-2-hydroxyglutarate, which is proposed to cause tumorigenesis. The production of this metabolite also causes vulnerabilities in cellular metabolism, such as lowering NADPH levels. To exploit this vulnerability, we treated glioma and fibrosarcoma cells that harbor an IDH1 mutation with an inhibitor of nicotinamide adenine dinucleotide (NAD+) salvage pathway, FK866, and observed decreased viability in these cells. To understand the mechanism of action by which the inhibitor FK866 works, we used Raman imaging microscopy and identified that proteins and lipids are decreased upon treatment with the drug. Raman imaging showed a different distribution of lipids throughout the cell in the presence of the drug compared with the untreated cells. We employed nuclear magnetic resonance NMR spectroscopy and mass spectrometry to identify the classes of lipids altered. Our combined analyses point to a decrease in cell division due to loss of lipid content that contributes to membrane formation in the in vitro setting. However, the FK866 drug did not have the same potency in vivo. The use of Raman imaging microscopy indicated an opposite trend of lipid distribution in the tissue collected from treated versus untreated mice when compared with the cells. These results demonstrate the role of Raman imaging microscopy to identify and quantify metabolic changes in cancer cells and tissue.

EFFECT OF GROWTH HORMONE AND PEPTIDE FRACTIONS CONTAINING SOMATOMEDIN ACTIVITY ON GROWTH AND CARTILAGE METABOLISM OF SNELL DWARFMICE

1979 ◽  
Vol 92 (2) ◽  
pp. 242-257 ◽  
Author(s):  
Sylvia van Buul-Offers ◽  
Jan Leo Van den Brande ◽  
C. M. Hoogerbrugge ◽  
L. Dumoleijn ◽  
P. L. M. v.d. Klundert
Keyword(s):  
Growth Hormone ◽  
Thymidine Incorporation ◽  
Costal Cartilage ◽  
Human Growth ◽  
Liver Weight ◽  
Skinfold Thickness ◽  
Treated Group ◽  
Serum Glucose ◽  
Significant Rise

ABSTRACT In order to obtain more information about a possible role of somatomedin (SM) in vivo, increase in length and weight, costal cartilage activity (35SO4 = and 3H-methyl-thymidine incorporation), organ weight and serum glucose levels were studied in Snell dwarfmice, during treatment with human growth hormone (hGH), l-thyroxine (T4), insulin and a semipurified SM-preparation (SM-P1). SM-P1, hGH and T4 caused a significant increase in length and weight, whereas insulin was not effective in a dosage similar to the insulinlikeactivity of the SM-P1 preparation measured by radioreceptorassay. The effect obtained with the SM-preparation cannot be due to contamination of GH, prolactin, T4, insulin or testosterone. Costal cartilage activity was measured three days after initiation of treatment by incubation immediately after sacrifice in plasma free medium. Both sulphate and thymidine incorporation were increased by the administration of SM-Pl and hGH, compared to buffer treated controls. After treatment for four weeks no differences between treated and untreated animals in cartilage activity could be observed anymore. Both SM-P1 and hGH induced weight gain in most organs. An outspoken effect was seen on lymphoid organs, the submandibular salivary glands and muscle, a sizable effect was present on the kidneys and a small effect, not reaching significance for the SM-Pl treated group on brain weight. An impression of divergence was seen with liver weight, which increased on hGH while there was a small and not significant rise on SM-P1. A definite discrepancy was found in skinfold thickness, which was essentially unchanged on hGH and increased on SM-P1. Testes and epididymal fat, though probably increasing their weights, were in insufficient number to do statistics on. Serum T4 is low in untreated dwarfmice. It is increased to a subnormal level after hGH administration whereas no effect is observed with SM-P1. The dose dependent effect of insulin, measured by radioimmunoassay, on the induction of hypoglycaemia is markedly similar to the effect of nonradioimmunoactive insulin-like activity of SM-P1 as measured by radioreceptorassay. The hypoglycaemia induced with insulin and the SM-preparation is reduced by adding 10 % glucose to the diet. In conclusion: SM-P1 shows growth stimulating and insulin-like actions in vivo. The pattern of effects obtained with hGH, T4 and insulin differs from that of SM-P1.

scholarly journals Analysis of the effect of leptin on immune function in vivo using diet-induced obese mice

2004 ◽  
Vol 180 (1) ◽  
pp. 167-173 ◽  
Author(s):  
N Mito ◽  
H Yoshino ◽  
T Hosoda ◽  
K Sato
Keyword(s):  
Immune Function ◽  
Standard Diet ◽  
Lymphocyte Function ◽  
Immune Functions ◽  
Obese Mice ◽  
Free Feeding ◽  
And Control ◽  
Phosphate Buffered Saline

Leptin can regulate several immune functions. However, the role of leptin on lymphocyte function has not been recognized in vivo. Accordingly, we have investigated the effect of leptin on starvation-induced immune dysfunction using diet-induced obese mice. To induce obesity, C57BL/6J mice were fed a high-fat diet for 14 weeks and control mice were fed a standard diet for the same period. The obese and control groups of mice were then starved for 48 h, and received intraperitoneal injections of recombinant leptin or phosphate-buffered saline four times during starvation. Other control mice in both diet groups were free fed without being starved. Although starvation of the control mice dramatically reduced the weights of the immune organs, cytokine production and increased proliferation of cultured splenocytes, these levels returned to those of the free-feeding groups with exogenous leptin administration. However, these effects of leptin were not observed in obese mice. These findings provide some evidence that leptin can regulate the immune function in vivo. It is also suggested that the action of leptin might not appear in obesity.

scholarly journals Comparison of Sulfate Metabolism in Costal Cartilage of Normal and 'Little' Mice

1983 ◽  
Vol 36 (3) ◽  
pp. 263 ◽  
Author(s):  
NeiI M McKern
Keyword(s):  
Growth Hormone ◽  
Growth Rate ◽  
Body Weight ◽  
Costal Cartilage ◽  
Cartilage Degradation ◽  
Skeletal Growth ◽  
Sulfate Uptake ◽  
Sulfate Metabolism ◽  
C 50

C57BL/6J and mutant 'little' (lit/lit) mice c. 50 days of age were injected with doses of [35S]sulfate proportional to their body weight. Despite the diminished growth rate of lit/lit mice compared with normal mice at this age, uptake of radioactivity per unit mass of cartilage was similar for both mouse types, confirming previous data. Additional experiments with these mice established that the similarity of sulfate uptake could not be accounted for by differences in the location of bound sulfate or (for females) by differences in cartilage cellularity. Investigation of sulfate loss by costal cartilage in vivo indicated that cartilage degradation occurred at a greater rate in lit/lit mice than in normally growing mice. These latter data suggest that growth hormone, which is lacking in lit/lit mice, may in part regulate skeletal growth (at least for female mice) by inhibiting degradation of cartilage.

scholarly journals Sulfate Uptake and Somatomedin Levels in the 'Little' (lit/lit) Mouse

1981 ◽  
Vol 34 (2) ◽  
pp. 221 ◽  
Author(s):  
NeiI M McKern ◽  
Donald B Cheek ◽  
WGordon Crewther
Keyword(s):  
Growth Hormone ◽  
Costal Cartilage ◽  
Fresh Medium ◽  
Bovine Growth Hormone ◽  
Consistent Difference ◽  
Sulfate Uptake ◽  
Low Levels ◽  
In Vivo Uptake

The mutant 'little' (lit/lit) mouse is deficient in growth hormone and has correspondingly low levels of serum somatomedin. Injection of these mice with human or bovine growth hormone significantly r(l.ises serum somatomedin levels within 6 h. In vivo uptake of radioactive sulfate by costal cartilage in lit/lit mice is similar to that of normal mice, which is unexpected in view of the low levels of circulating somatomedin. If costal cartilages from normal and lit/lit mice are preincubated in medium 199 in vitro before transfer to fresh medium containing radioactive sulfate and serum, there is no consistent difference in uptake of sulfate, demonstrating similar endogenous cartilage activity. In contrast, omission of the preincubation step reveals a lower uptake of sulfate in vitro by cartilage from lit/lit mice as compared with normal mice. Cartilage removed from lit/lit mice 24 h after injection with growth hormone, however, takes up greater amounts of sulfate than cartilage from untreated normal mice.

Metabolic Changes in Human CD36 Deficiency Displayed by Glucose Loading

2001 ◽  
Vol 86 (10) ◽  
pp. 995-999 ◽  
Author(s):  
Hidekatsu Yanai ◽  
Hironobu Fujiwara ◽  
Mie Morimoto ◽  
Yukihiro Takahashi ◽  
Shu-Ping Hui ◽  
...  
Keyword(s):  
Metabolic Changes ◽  
Type I ◽  
Type Ii ◽  
Loading Test ◽  
Glucose Loading ◽  
Cd36 Deficiency ◽  
Metabolic Role

SummaryPrevious in vitro studies have shown that CD36 participates in cellular fatty acid (FA) uptake. In vivo evidence for a physiologic role of CD36 in this process is poor and mostly obtained in animals. To examine the metabolic role of human CD36, we performed a glucose loading test for normals (n = 16) and subjects with CD36 deficiency, both Type I (n = 5) and Type II (n = 16). After 30 min, FA levels had fallen by 60.1% in normals but by only 31.7% in Type II deficiency (P <0.01 vs. normals) and 16.5% in Type I deficiency which remained significantly higher than the other two groups out to 2 h. Further, changes in triglyceride and glucose metabolism were observed in the both types of CD36 deficiency. Impaired fast FA clearance by muscle and consequently increased hepatic FA uptake seem to underlie these changes. We conclude that human CD36 deficiency causes systemic metabolic changes.

scholarly journals Growth Hormone Receptor Gene is Essential for Chicken Mitochondrial Function In Vivo and In Vitro

2019 ◽  
Vol 20 (7) ◽  
pp. 1608 ◽  
Author(s):  
Bowen Hu ◽  
Shuang Hu ◽  
Minmin Yang ◽  
Zhiying Liao ◽  
Dexiang Zhang ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Growth Hormone ◽  
Mitochondrial Function ◽  
Hormone Receptor ◽  
Growth Hormone Receptor ◽  
Ghr Gene ◽  
Chicken Skeletal Muscle

The growth hormone receptor (GHR) gene is correlated with many phenotypic and physiological alternations in chicken, such as shorter shanks, lower body weight and muscle mass loss. However, the role of the GHR gene in mitochondrial function remains unknown in poultry. In this study, we assessed the function of mitochondria in sex-linked dwarf (SLD) chicken skeletal muscle and interfered with the expression of GHR in DF-1 cells to investigate the role of the GHR gene in chicken mitochondrial function both in vivo and in vitro. We found that the expression of key regulators of mitochondrial biogenesis and mitochondrial DNA (mtDNA)-encoded oxidative phosphorylation (OXPHOS) genes were downregulated and accompanied by reduced enzymatic activity of OXPHOS complexes in SLD chicken skeletal muscle and GHR knockdown cells. Then, we assessed mitochondrial function by measuring mitochondrial membrane potential (ΔΨm), mitochondrial swelling, reactive oxygen species (ROS) production, malondialdehyde (MDA) levels, ATP levels and the mitochondrial respiratory control ratio (RCR), and found that mitochondrial function was impaired in SLD chicken skeletal muscle and GHR knockdown cells. In addition, we also studied the morphology and structure of mitochondria in GHR knockdown cells by transmission electron microscopy (TEM) and MitoTracker staining. We found that knockdown of GHR could reduce mitochondrial number and alter mitochondrial structure in DF-1 cells. Above all, we demonstrated for the first time that the GHR gene is essential for chicken mitochondrial function in vivo and in vitro.

Sign in / Sign up

Export Citation Format

Share Document