Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0038187 (starvation)
 24,951 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Maternal and fetal plasma ovine placental lactogen (oPL), insulin, and IGF-I levels were measured in response to the starvation and refeeding of pregnant sheep on two defined planes of nutrition. Chronically catheterized pregnant ewes were placed on either a high plane (n = 5) or low plane (n = 5) of nutrition at least 1 wk before the experiment. At 125 to 135 d gestation, the ewes were starved for 72 h and then an i.v. infusion of 10% glucose was administered over 4 h, followed by refeeding at the designated nutritional plane. Plasma oPL levels of fetuses whose mothers had been on a high plane of nutrition were significantly higher during starvation (p less than 0.05) than those of fetuses whose mothers had been on a low plane (high + 0.54 +/- 0.17 and low -0.02 +/- 0.17 nmol/L from mean control levels). Intravenous glucose infusion to the ewes at the end of starvation caused a marked rise in fetal plasma oPL levels in both groups (increments of 2.61 +/- 1.4 nmol/L in the high group and 2.81 +/- 1.16 nmol/L in the low group). Maternal oPL levels did not differ significantly between the two nutritional groups during starvation and did not change during glucose infusion. Fetal and maternal plasma IGF-I levels both fell during starvation. Maternal IGF-I levels fell faster in the high group (-17.9 +/- 4.5 at 24 h versus -4.7 +/- 7.2 nmol/L in the low group), but the groups were not different at the end of starvation.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:The nutritional regulation of circulating placental lactogen in fetal sheep. 160 32

This study was undertaken to investigate the mechanisms by which an infusion of recombinant human insulin-like growth factor I (rhIGF-I) increases GFR and renal plasma flow (RPF) in rats. Glomerular micropuncture studies were carried out in 14 nonstarved Munich Wistar rats and in 12 rats deprived of food for 60-72 h. Animals were given an intravenous injection and infusion of either rhIGF-I or vehicle. In both nonstarved and starved animals, the IGF-I injection and infusion increased the serum IGF-I levels, left kidney GFR, single nephron glomerular filtration rate (SNGFR), single nephron blood flow rate (SNBF), and single nephron plasma flow rate (SNPF). The increase in SNPF and SNGFR was in part due to a fall in efferent arteriolar resistance (RE); there was a tendency, not significant, for afferent arteriolar resistance (RA) to fall in comparison to controls. The increase in SNGFR was partly caused by a rise in SNPF but was primarily due to an increase in glomerular ultrafiltration coefficient (LpA) to twice the control values. The increase in LpA resulted in an increase in SNGFR because the rats operated at ultrafiltration pressure disequilibrium. Control starved as compared with nonstarved rats had lower SNGFR, SNBF, and SNPF. This reduction was due to a tendency, not significant, for both RA and RE to be higher. Decreased SNGFR in food-deprived rats resulted from a reduced SNPF, a lower glomerular transcapillary hydrostatic pressure difference (delta P), and possibly a somewhat reduced LpA. These data indicate that IGF-I increases SNGFR, SNPF, and SNBF primarily by increasing LpA and also by decreasing RE without affecting delta P. Short-term starvation lowers SNGFR, SNPF, and SNBF primarily by decreasing delta P and possibly by lowering LpA and increasing RA and RE. IGF-I reverses some of the glomerular hemodynamic effects of short-term food deprivation.
 ...
PMID:Effects of recombinant human insulin-like growth factor I on glomerular dynamics in the rat. 201 May 36

In view of the suggested relationship between substrate availability, fetal growth and circulating fetal IGF-I concentrations, we investigated the effect of maternal starvation on plasma IGF-I levels in the late gestation ovine fetus. Ten fetuses aged 125-130 d gestation were sampled daily from indwelling arterial catheters. Ewes were starved for 72 h. Starvation was terminated with an intravenous infusion of 10% glucose to the ewe. Food was then replaced 4 h later. Fetal IGF-I concentrations fell from 176.1 +/- 15.2 ng/mL before starvation to 124.5 +/- 10.3 ng/mL after 72 h starvation (p less than 0.05, n = 10). The fall in IGF-I concentrations was reversed by 4 h of maternal glucose infusion. In five fetuses, where samples were obtained 24 h after terminating the starvation, fetal IGF-I concentrations were comparable to those seen before starvation (180.0 +/- 37.7 ng/mL). This study demonstrates that acute maternal starvation causes a reversible decrease in fetal plasma IGF-I levels. These studies suggest that nutrient and in particular glucose availability is a significant determinant of fetal IGF-I secretion and support the hypothesis that IGF-I may play a role in the regulation of fetal growth.
 ...
PMID:The effect of maternal starvation on plasma insulin-like growth factor I concentrations in the late gestation ovine fetus. 234 30

Insulin-like growth factor I (IGF-I, somatomedin C) was mapped by immunocytochemistry in the pancreas of normal and experimentally influenced rats. The polyclonal IGF-I antiserum K 37 was characterized and demonstrated to be specific. In the exocrine pancreas some duct cells showed IGF-I immunoreactivity, other components being negative. The three main endocrine cell types in the islets of Langerhans were IGF-I immunoreactive, most strikingly the D cells. Hypophysectomy resulted in loss of IGF-I immunoreactivity in all three endocrine cell types, i.e. D, A and B cells, while the levels of somatostatin, glucagon and insulin, respectively, remained unchanged. Starvation seemed to increase and feeding to decrease the IGF-I immunoreactivity in the B cells. Cysteamine pre-treatment reduced the normally intense IGF-I and somatostatin immunoreactivities in the D cells. In rats made diabetic with alloxan or streptozotocin, the B cells were irreversibly damaged and lost both their insulin and IGF-I immunoreactivities, while the IGF-I immunoreactivity was increased in A cells; the D cells remained unchanged. The concentrations of IGF-I mRNA in the pancreas were almost equal in normal and alloxan diabetic rats as were the concentrations of extractable IGF-I. We conclude that IGF-I immunoreactive material can be demonstrated in adult animals in all endocrine islet cells, most prominently in the D cells. The expression of IGF-I immunoreactivity is in part under pituitary control. In the adult rat only one islet cell type synthesizes IGF-I immunoreactive material, i.e. the D cells, while, in contrast, the B cells are likely to be a major IGF-I source in fetal and neonatal islets.
 ...
PMID:Insulin-like growth factor I in the pancreas of normal and diabetic adult rats. 246 68

Starvation, glucagon and cyclic AMP inhibit, and refeeding starved animals and insulin or IGF-I plus triiodothyronine stimulate accumulation of FAS and its mRNA in liver; transcription is the primary regulated step. In the uropygial gland, differentiation of basal cells into mature sebocytes is accompanied by the accumulation of large amounts of FAS and its mRNA. By analogy with liver, transcription is likely to be the regulated step, but direct experimental evidence for this hypothesis is lacking. FAS mRNA is a unique gene and is probably more than 100 kb in length. The FAS gene of goose and duck is transcribed into two mature mRNAs of about 10,800 and 12,200 nucleotides. The 3'-untranslated regions of the FAS mRNAs contain an unusual polypyrimidine tract which, at the mRNA level at least, appears unrelated to regulation of gene expression. Polypyrimidine tracts similar in sequence to that in the FAS gene are found in about 20 different parts of the genome. All of the fragments which contain these tracts are hypermethylated. The next stage of this investigation will involve identification of cis-acting sequence elements in the FAS gene which specify responses to diet, hormones and tissue-specific regulatory factors. Isolation and characterization of the 5'-ends of the cDNA and the gene are underway.
 ...
PMID:Structure and regulation of the avian gene for fatty acid synthase. 259 Mar 94

Immunocytochemical, immunochemical and RNA-hybridization techniques were used to map the distribution of somatomedin C (Sm-C; insulin-like growth factor I; IGF-I) in the pancreas of young and adult lean and obese mice. The D cells in the islets of Langerhans showed intense cytoplasmic Sm-C immunoreactivity, extending into their processes. Only slight Sm-C immunoreactivity was seen in A and B cells, apparently confined to the plasma membranes. In the exocrine pancreas scattered duct cells were immunopositive. Starvation increased, while feeding decreased the Sm-C immunoreactivity in B cells. RNA-hybridization analyses revealed that roughly the same number of Sm-C mRNA molecules, as calculated per DNA amount in the pancreas, could be demonstrated in young and adult, lean and obese mice. Radioimmunoassay (RIA) determinations of total Sm-C showed that there were about equal concentrations in the pancreas of lean and obese mice. There were marked differences between the liver and the pancreas, in that the RIA Sm-C values for the former were twice those in the latter while, in contrast, the corresponding values for the Sm-C mRNA, i.e. the agent determining the synthesis of Sm-C, were about 100 times higher in the liver as compared to that in the pancreas. We interpret our results as follows: The D cells in the islets form and secrete Sm-C in both young and adult, lean and obese mice, while A and B cells bind, but do not necessarily synthesize this peptide.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Somatomedin C in the pancreas of young and adult, normal and obese, hyperinsulinemic mice. 292 45

The pattern of cellular protein glycosylation can be altered in CHO cells by glucose starvation. When wild type CHO cells are deprived of glucose, 125I-insulin binding increases from a B/F of 0.033 +/- 0.004 to 0.063 +/- 0.011, due to an increase in receptor affinity. The already elevated insulin binding to mutant B4-2-1 CHO cells, whose genetic defect causes abnormal glycosylation mimicking the pattern seen in the glucose starved normal cells, is not affected by glucose starvation. In neither cell line is 125I-IGF-I binding affected by glucose starvation. These data support the hypothesis that abnormal glycosylation can alter insulin binding to its receptor. Furthermore, there is a striking difference in the susceptibility of IGF-I and insulin receptors to alterations in glycosylation.
 ...
PMID:Glucose starvation alters insulin but not IGF-I binding to Chinese hamster ovary (CHO) cells. 353 97

Insulin-like growth factor-II (IGF-II) is an important regulator of embryonic growth and differentiation, but its function in postnatal life is unclear. To address this point, we generated transgenic mice harboring fusion genes in which a human IGF-II complementary DNA is placed under the transcriptional control of the rat phosphoenolpyruvate carboxykinase promoter. Transgene-specific messenger RNA was detected in liver, kidney, and several parts of the gut. Serum IGF-II levels in transgenic mice were 2-3 times higher than those in controls and increased after starvation. Circulating IGF-I correlated negatively and IGF-binding protein-2 (IGFBP-2) positively with IGF-II levels, suggesting that IGF-I is displaced from IGFBPs by IGF-II and that IGF-II is a major regulator of IGFBP-2. Serum levels of IGFBP-3 and IGFBP-4 tended to be higher in phosphoenolpyruvate carboxykinase-IGF-II transgenic mice than in controls, as evaluated by ligand blot analysis. Starvation reduced serum IGF-I, but increased IGFBP-2 in transgenic mice more markedly than in controls. Fasting insulin levels were significantly reduced in transgenic mice, whereas glucose levels were not influenced by elevated IGF-II. The body growth of 4- and 12-week-old mice was not significantly influenced by elevated IGF-II, but transgenic mice displayed increased kidney and testis weight at the age of 4 weeks, and increased adrenal weight at the age of 12 weeks. Our results demonstrate that elevated IGF-II in postnatal life has multiple endocrine consequences and subtle time-specific effects on organ growth.
 ...
PMID:Consequences of postnatally elevated insulin-like growth factor-II in transgenic mice: endocrine changes and effects on body and organ growth. 752 57

The IGF regulatory system has been shown to mediate mitogenic effects during normal growth and tumor proliferation. The bioavailability of both IGF-I and IGF-II is regulated by at least six specific IGF binding proteins (IGFBPs). Whereas IGFBP-3 is the main IGFBP postnatally, IGFBP-2 is the predominant IGFBP during fetal life. In addition, IGFBP-2 is expressed in a range of tumor cell lines. In order to investigate the IGF regulatory pathway in malignancies we analyzed by RIA serum samples of 49 children with leukemia, Non-Hodgkins' Lymphoma (NHL) or solid tumors at the time of diagnosis. Serum concentrations of IGF-I (mean/range: -2.4/0.3 to -9.9 SDS), IGF-II (-2.5/0.2 to -5.6 SDS) and IGFBP-3 (-1.3/2.2 to -6.8 SDS) were significantly decreased, but IGFBP-2 (3.2/-0.9 to 8.6 SDS) was elevated. Both absolute as well as SDS values of IGF-I, -II and the sum of IGF-I and IGF-II (r = -0.49, p < 0.01) were inversely correlated with IGFBP-2. Serum levels of the growth factors IGF-I and IGF-II were significantly decreased in different types of malignancies to concentrations usually seen only in patients with growth hormone deficiency or during starvation. However, the elevated levels of IGFBP-2 in 70% of our patients exceeded by far those in growth hormone deficiency. Furthermore, in this study we could demonstrate that serum levels of IGF-I and IGF-II were inversely correlated to IGFBP-2 independent on the type of malignancy, indicating a common regulatory mechanism of the IGF signaling pathway in these diseases.
 ...
PMID:[Serum concentrations of insulin-like growth factors (IGF)-I and IGF-II and IGF binding proteins (IGFBP)-2 and IGFBP-3 in 49 children with ALL, NHL or solid tumors]. 756 58

The influence of fetal glucose and amino acid supply on the regulation of fetal plasma IGF-I levels was investigated in fetuses from starved ewes. Paired maternal and fetal blood samples were taken during an initial 2-d control period, after 48 h of maternal starvation, during a 24-h fetal infusion of glucose (n = 6) or an amino acid mixture (Synthamin 17, n = 5) with continued starvation, and after 48 h of maternal refeeding. After 48 h of starvation, maternal and fetal plasma IGF-I, insulin, and blood glucose fell significantly in both groups compared with control values (IGF-I for glucose group: maternal, -18.53 +/- 6.60; fetal, -5.23 +/- 1.81 nmol/L; amino acid group: maternal, -18.2 +/- 6.97, fetal, -5.12 +/- 1.61 nmol/L; both p < 0.05). Fetal glucose but not mixed amino acid infusion raised fetal plasma IGF-I, insulin, and blood glucose to near control values (glucose group fetal IGF-I, -1.77 +/- 1.98; amino acid group, -5.93 +/- 2.22 nmol/L; both p < 0.05). Maternal plasma IGF-I remained depressed during glucose infusion (-16.33 +/- 8.32 nmol/L), but continued to fall in the amino acid group (-21.41 +/- 8.20 nmol/L, p < 0.05). After 48 h of maternal refeeding, all values had returned to near control values for both groups (glucose group IGF-I: maternal, -5.2 +/- 3.86; fetal, 0.01 +/- 2.2; nmol/L; amino acid group: maternal, -11.66 +/- 3.2; fetal, -0.70 +/- 2.61 nmol/L). We conclude that in the ovine fetus glucose may have a more important role than amino acids in the regulation of fetal plasma IGF-I.
 ...
PMID:Glucose but not a mixed amino acid infusion regulates plasma insulin-like growth factor-I concentrations in fetal sheep. 835 21


1 2 3 4 5 6 Next >>