cholecalciferol has been researched along with Hypertrophy* in 8 studies
8 other study(ies) available for cholecalciferol and Hypertrophy
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Delving into disability in Crohn's disease: dysregulation of molecular pathways may explain skeletal muscle loss in Crohn's disease.
In Crohn's disease (CD), skeletal muscle mass and function are reduced compared to healthy controls, potentially resulting in disability. Mechanisms contributing to muscle impairment, and thus potential therapeutic targets, are poorly understood. This study aimed to measure and compare skeletal muscle size and molecular targets involved in skeletal muscle growth, in CD subjects and healthy controls.. CD (n=27) and healthy (n=22) subjects were recruited from the IBD outpatient clinic and via local advertisement respectively. Demographics and clinical data were collected via survey and interview. Quadriceps muscle cross-sectional area was measured using peripheral quantitative CT scanning. Levels of muscle hypertrophy and atrophy signalling targets using quantitative PCR and western blotting were measured in muscle biopsies.. Muscle size was 14% lower (p=0.055) and a 54% lower phosphorylated:total (p:t) Akt ratio was measured in the muscle samples (p<0.05), indicating an attenuated muscle hypertrophy pathway in CD compared with controls. In those with CD, a lower p:t Akt ratio (<0.97) was associated with lower serum vitamin D3, lower physical activity indices (49 vs 64 mmol/L, 1.7 vs 2.2×10(6) accelerometer counts respectively, each p<0.05) and a trend towards lower serum ferritin levels (128 vs 322mg/L, p=0.07), compared with CD subjects with normal/high p:t Akt ratios.. The reduced muscle mass in CD may be explained, in part, by impaired activation of muscle protein synthesis pathways, notably the IGF1-Akt pathway. Normal vitamin D levels and regular exercise may be protective in CD against this trend, though confirmatory longitudinal studies are needed. Topics: Adaptor Proteins, Signal Transducing; Adult; Biopsy; Cell Cycle Proteins; Cholecalciferol; Crohn Disease; Cross-Sectional Studies; Female; Ferritins; Humans; Hypertrophy; Insulin-Like Growth Factor I; Interleukin-6; Male; Middle Aged; Motor Activity; Muscular Atrophy; Organ Size; Phosphoproteins; Phosphorylation; Protein Tyrosine Phosphatases; Proto-Oncogene Proteins c-akt; Quadriceps Muscle; Signal Transduction | 2014 |
Ultrastructure of thyroid C cells in sheep treated with vitamin D3.
Ultrastructural observation was performed in C cells of sheep injected intramuscularly with a dose of 2 million IU of vitamin D3 daily for 10 days, 20 days and 30 days, respectively. After treatment with vitamin D3, hyperplasia and hypertrophy of C cells were noticed mainly at the periphery of the thyroid follicles. Most of hypertrophied C cells degranulated conspicuously and contained many prosecretory granules near the well developed Golgi apparatus which were in the actively secreting and packaging phase of their secretory cycle. The other C cells had prominent lamellar arrays of rough-endoplasmic reticulum and aggregations of free ribosomes in the cytoplasm which were interpreted to be in the actively synthesizing phase of their secretory cycle. Atrophic C cells which contained degenerative organelles in the cytoplasm were occasionally observed among the hypertrophied C cells. The present ultrastructural findings clarified that C cells synthesize and secrete calcitonin continuously due to prolonged hypercalcemia induced by long-term administration of excessive doses of vitamin D3 in sheep. Topics: Animals; Cholecalciferol; Cytoplasmic Granules; Endoplasmic Reticulum; Golgi Apparatus; Hyperplasia; Hypertrophy; Injections, Intramuscular; Male; Microscopy, Electron; Mitochondria; Ribosomes; Sheep; Thyroid Gland | 1991 |
Immunohistochemical alterations of C cells in sheep treated with vitamin D.
Hyperplasia and hypertrophy of C cells were demonstrated in sheep with hypercalcaemia induced by administration of vitamin D3 (2 million I.U. per day). After treatment with vitamin D3 for 10, 20 or 30 days, serum calcium values increased to 10.28, 11.86 and 10.44 mg per dl, respectively, compared to a normal concentration of around 9 mg per dl. Immunohistochemical reactions of calcitonin, chromogranin A and calcitonin gene-related peptide (CGRP) decreased, whereas intense neurone-specific enolase (NSE) immunoreactivity was noted in C cells. Immunohistochemical staining with anti-calcitonin, anti-chromogranin A, anti-CGRP and anti-NSE antisera was useful to demonstrate the functional state of stimulated C cells in sheep with hypercalcaemia. Topics: Animals; Calcitonin; Calcitonin Gene-Related Peptide; Calcium; Cholecalciferol; Chromogranin A; Chromogranins; Hypercalcemia; Hyperplasia; Hypertrophy; Phosphopyruvate Hydratase; Sheep; Thyroid Gland | 1991 |
Immunohistochemical alterations on thyroid C cells of rabbits treated with vitamin D3.
Topics: Animals; Calcitonin; Calcitonin Gene-Related Peptide; Cholecalciferol; Chromogranin A; Chromogranins; Hyperplasia; Hypertrophy; Immunohistochemistry; Male; Phosphopyruvate Hydratase; Rabbits; Somatostatin; Thyroid Gland | 1991 |
Structure and behaviour of ultimobranchial gland in response to vitamin D3--induced hypercalcemia in male Clarias batrachus.
Hypercalcemia was induced in Clarias batrachus by treating them with vitamin D3 (5,000 I.U./100 g body wt.) and/or 0.5% solution of CaCl2. The animals were killed on 1st, 3rd, 5th, 9th, 13th and 17th days after the initiation of the experiment. Histological preparations of the ultimobranchial gland (UBG) were made. The gland exhibits nuclear hypertrophy, hyperplasia and loss of staining response corresponding to the rise in serum calcium levels. At later intervals, the UBG shows exhaustion and degeneration which is evident from vacuolization and nuclear shrinkage of the ultimobranchial cells after day 13 in groups B and C and day 9 in group D. Topics: Animals; Calcium Chloride; Cholecalciferol; Fishes; Hyperplasia; Hypertrophy; Male; Staining and Labeling; Time Factors; Ultimobranchial Body | 1984 |
The bone inductive capacity of decalcified bone matrix modified by diphenylhydantoin.
Decalcified bone matrix was prepared from cortical bones of rats premedicated with I) Diphenylhydantoin (DPH), II) DPH + Vitamin D3, III) Vitamin D3 or IV) no premedication for 10 days. In the donor animals, DPH lowered the serum calcium level, caused a weight loss of 10 per cent, and stopped the growth of the long bones. Vitamin D3 supplementation normalized the serum calcium concentration but had no effect on the other parameters. Vitamin D3 alone caused hypertrophy of the growth cartilage, while the bone growth and structure was normal. The bone inductive capacity of decalcified bone matrix was highest in the DPH group, and the DPH + D3 group also showed significantly higher values than the D3, and control groups. The results of the present study show that the bone inductive capacity of the decalcified bone matrix is independent of Vitamin D3 metabolism. Topics: Animals; Body Weight; Bone Development; Bone Matrix; Calcium; Cartilage; Cholecalciferol; Hypertrophy; Male; Phenytoin; Rats; Rats, Inbred Strains | 1981 |
Electron microscopic studies on the parafollicular cells and parafollicular cell complexes in the dog.
Topics: Animals; Calcitonin; Calcium; Cholecalciferol; Chromatin; Cytoplasm; Dogs; Endoplasmic Reticulum; Epithelial Cells; Female; Glycogen; Histocytochemistry; Hypercalcemia; Hyperplasia; Hypertrophy; Male; Microscopy, Electron; Parathyroid Glands; Thyroid Gland | 1973 |
Vitamin D-actinomycin D interactions in bone. An electron microscopic study of hypertrophy and hyperinvolution of osteoblasts.
Topics: Animals; Bone and Bones; Cholecalciferol; Dactinomycin; Hypertrophy; Microscopy, Electron; Osteoblasts; Rats | 1966 |