scholarly journals Up-regulation of liver glucose-6-phosphatase in rats fed with a Pi-deficient diet

1999 ◽  
Vol 343 (2) ◽  
pp. 393-396 ◽  
Author(s):  
Wensheng XIE ◽  
Yazhou LI ◽  
Marie-Claire MÉCHIN ◽  
Gérald VAN DEWERVE
Keyword(s):  
Glycogen Content ◽  
Control Diet ◽  
Liver Microsomes ◽  
Catalytic Subunit ◽  
Protein Abundance ◽  
Deficient Diet ◽  
Pi Transport ◽  
Nutritional Conditions ◽  
G6pase Activity ◽  
Pi Deficiency

Because Pi deprivation markedly affects the Na/Pi co-transporter in kidney and has been related to insulin resistance and glucose intolerance, the effect of a Pi-deficient diet on the liver microsomal glucose-6-phosphatase (G6Pase) system was investigated. Rats were fed with a control diet (+Pi) or a diet deficient in phosphate (-Pi) for 2 days and killed on the morning of the third day, after an overnight fast (fasted) or not (fed). Kinetic parameters of Pi transport (t½ and equilibration) into liver microsomes were not changed by the different nutritional conditions. In contrast, it was found that G6Pase activity was significantly increased in the (-Pi) groups. This was due to an increase in the Vmax of the enzyme, without change in the Km for G6P. There was no correlation between liver microsomal glycogen content and G6Pase activity, but both protein abundance and mRNA of liver 36 kDa catalytic subunit of G6Pase (p36) were increased. The mRNA of the putative G6P translocase protein (p46) was changed in parallel with that of the catalytic subunit, but the p46 immunoreactive protein was unchanged. These findings indicate that dietary Pi deficiency causes increased G6Pase activity by up-regulation of the expression of the 36 kDa-catalytic-subunit gene.

Diets enriched in sucrose or fat increase gluconeogenesis and G-6-Pase but not basal glucose production in rats

2002 ◽  
Vol 283 (3) ◽  
pp. E545-E555 ◽  
Author(s):  
S. Renee Commerford ◽  
Jennifer B. Ferniza ◽  
Michael E. Bizeau ◽  
Jeffrey S. Thresher ◽  
Wayne T. Willis ◽  
...  
Keyword(s):  
Control Diet ◽  
Liver Microsomes ◽  
Glucose Production ◽  
Catalytic Subunit ◽  
Glucose Phosphorylation ◽  
High Starch ◽  
High Sucrose ◽  
Fasted Rats

High-fat (HFD) and high-sucrose diets (HSD) reduce insulin suppression of glucose production in vivo, increase the capacity for gluconeogenesis in vitro, and increase glucose-6-phosphatase (G-6-Pase) activity in whole cell homogenates. The present study examined the effects of HSD and HFD on in vivo gluconeogenesis, the catalytic and glucose-6-phosphate translocase subunits of G-6-Pase, glucokinase (GK) translocation, and glucose cycling. Rats were fed a high-starch control diet (STD; 68% cornstarch), HSD (68% sucrose), or HFD (45% fat) for 7–13 days. The ratio of3H in C6:C2 of glucose after3H2O injection into 6- to 8-h-fasted rats was significantly increased in HSD (0.68 ± 0.07) and HFD (0.71 ± 0.08) vs. STD (0.40 ± 0.10). G-6-Pase activity was significantly higher in HSD and HFD vs. STD in both intact and disrupted liver microsomes. HSD and HFD significantly increased the amount of the p36 catalytic subunit protein, whereas the p46 glucose-6-phosphate translocase protein was increased in HSD only. Despite increased nonglycerol gluconeogenesis and increased G-6-Pase, basal glucose and insulin levels as well as glucose production were not significantly different among groups. Hepatocyte cell suspensions were used to ascertain whether diet-induced adaptations in glucose phosphorylation and GK might serve to compensate for upregulation of G-6-Pase. Tracer-estimated glucose phosphorylation and glucose cycling (glucose ↔ glucose 6-phosphate) were significantly higher in cells isolated from HSD only. After incubation with either 5 or 20 mM glucose and no insulin, GK activity (nmol · mg protein−1· min−1) in digitonin-treated eluates (translocated GK) was significantly higher in HSD (32 ± 4 and 146 ± 6) vs. HFD (4 ± 1 and 83 ± 10) and STD (9 ± 2 and 87 ± 9). Thus short-term, chronic exposure to HSD and HFD increase in vivo gluconeogenesis and the G-6-Pase catalytic subunit. Exposure to HSD diet also leads to adaptations in glucose phosphorylation and GK translocation.

Dietary Calcium Supplementation Suppresses Bone Formation in Magnesium-Deficient Rats

2006 ◽  
Vol 76 (3) ◽  
pp. 111-116 ◽  
Author(s):  
Hiroshi Matsuzaki ◽  
Misao Miwa
Keyword(s):  
Bone Formation ◽  
Calcium Supplementation ◽  
Control Diet ◽  
Formation Rate ◽  
Dietary Calcium ◽  
Mineral Apposition Rate ◽  
Control Group ◽  
Deficient Diet ◽  
Bone Formation Rate ◽  
Male Wistar Rats

The purpose of this study was to clarify the effects of dietary calcium (Ca) supplementation on bone metabolism of magnesium (Mg)-deficient rats. Male Wistar rats were randomized by weight into three groups, and fed a control diet (control group), a Mg-deficient diet (Mg- group) or a Mg-deficient diet having twice the control Ca concentrations (Mg-2Ca group) for 14 days. Trabecular bone volume was significantly lower in the Mg - and Mg-2Ca groups than in the control group. Trabecular number was also significantly lower in the Mg - and Mg-2Ca groups than in the control group. Mineralizing bone surface, mineral apposition rate (MAR), and surface referent bone formation rate (BFR/BS) were significantly lower in the Mg - and Mg-2Ca groups than in the control group. Furthermore, MAR and BFR/BS were significantly lower in the Mg-2Ca group than in the Mg - group. These results suggest that dietary Ca supplementation suppresses bone formation in Mg-deficient rats.

Differential regulation of PHEX expression in bone and parathyroid gland by chronic renal insufficiency and 1,25-dihydroxyvitamin D3

2004 ◽  
Vol 286 (4) ◽  
pp. F739-F748 ◽  
Author(s):  
Angela J. Brewer ◽  
Lucie Canaff ◽  
Geoffrey N. Hendy ◽  
Harriet S. Tenenhouse
Keyword(s):  
Renal Insufficiency ◽  
Parathyroid Gland ◽  
Chronic Renal Insufficiency ◽  
Control Diet ◽  
Protein Abundance ◽  
Dihydroxyvitamin D3 ◽  
Dihydroxyvitamin D ◽  
Phex Gene ◽  
Rat Tibia ◽  
Serum Pth

Mutations in the PHEX gene are responsible for X-linked hypophosphatemia, a renal phosphate-wasting disorder associated with defective skeletal mineralization. PHEX is predominantly expressed in bones and teeth and in the parathyroid gland of patients with chronic renal failure and tertiary hyperparathyroidism. The purpose of the present study was to examine the effects of renal insufficiency and 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] on the regulation of PHEX expression in rat tibia and parathyroid gland. In rats fed a high-phosphate (Pi) diet, ⅚ nephrectomy elicited a significant increase in the serum parathyroid hormone (PTH) concentration that was associated with a significant increase in the abundance of PHEX mRNA and protein in the tibia and a significant increase in PHEX mRNA in the parathyroid gland. In contrast, 1,25(OH)2D3 administration to intact rats fed a control diet elicited a significant decrease in the serum PTH concentration that was accompanied by a significant decrease in PHEX mRNA and protein abundance in the tibia and a significant decrease in PHEX mRNA in the parathyroid gland. In addition, the increases in serum PTH levels and PHEX mRNA in the tibia and parathyroid gland in ⅚ nephrectomized rats fed a high-Pi diet were blunted by 1,25(OH)2D3. Serum PTH concentration was positively and significantly correlated with tibial PHEX mRNA and protein abundance. In summary, we demonstrate that PHEX expression in the tibia and parathyroid gland is increased by chronic renal insufficiency and decreased by 1,25(OH)2D3 administration and suggest that PTH status may play an important role in mediating these changes in PHEX expression.

Fluoxetine-induced changes in body weight and 5-HT1A receptor-mediated hormone secretion in rats on a tryptophan-deficient diet

2004 ◽  
Vol 286 (2) ◽  
pp. R390-R397 ◽  
Author(s):  
D. N. D'Souza ◽  
Y. Zhang ◽  
F. Garcia ◽  
G. Battaglia ◽  
L. D. Van de Kar
Keyword(s):  
Body Weight ◽  
Control Diet ◽  
Hormone Secretion ◽  
Significant Loss ◽  
Tryptophan Depletion ◽  
Deficient Diet ◽  
Hormone Responses ◽  
Plasma Hormones ◽  
Induced Changes ◽  
The Impact

Tryptophan depleting protocols are commonly used to study the role of serotonin in mood disorders. The present study examined the impact of a tryptophan-deficient diet and fluoxetine on the serotonergic regulation of neuroendocrine function and body weight. We hypothesized that the regulation of postsynaptic 5-HT1A receptors is dependent on the levels of 5-HT in the synapse. Rats on a control or a tryptophan-deficient diet received daily injections of saline or fluoxetine (5 or 10 mg·kg-1·day-1 ip) from day 7 to day 21. The tryptophan-deficient diet produced a 41% reduction in the level of 5-HT but no change in the density of [3H]paroxetine-labeled 5-HT transporters. Treatment with fluoxetine inhibited the gain in weight in rats maintained on the control diet. The tryptophan-deficient diet produced a significant loss in body weight that was not significantly altered by treatment with fluoxetine. Treatment with fluoxetine produced a dose-dependent desensitization of hormone responses to injection of the 5-HT1A receptor agonist (±)8-hydroxy-2-(di- n-propylamino)tetralin ((±)8-OH-DPAT). The tryptophan-deficient diet produced an increase in the basal levels of corticosterone but did not alter the basal levels of ACTH or oxytocin. Also, this diet inhibited the magnitude of 8-OH-DPAT-induced increase in plasma levels of ACTH and oxytocin but did not impair the ability of fluoxetine to desensitize the 5-HT1A receptor-mediated increase in plasma hormones. These data suggest that a reserve of 5-HT enables fluoxetine to desensitize postsynaptic 5-HT1A receptors in the hypothalamus. In conclusion, the profound physiological changes induced by tryptophan depletion may complicate the interpretation of studies using this experimental approach.

scholarly journals Response of diamine oxidase and other plasma copper biomarkers to various dietary copper intakes in the rat and evaluation of copper absorption with a stable isotope

2000 ◽  
Vol 83 (5) ◽  
pp. 561-568 ◽  
Author(s):  
C. Feillet-Coudray ◽  
C. Coudray ◽  
D. Bayle ◽  
E. Rock ◽  
Y. Rayssiguier ◽  
...  
Keyword(s):  
Urinary Excretion ◽  
Intestinal Absorption ◽  
Diamine Oxidase ◽  
Control Diet ◽  
The Other ◽  
Control Group ◽  
Deficient Diet ◽  
Apparent Absorption ◽  
Cu Deficiency ◽  
Cu Isotope

There is a lack of agreement on index of Cu status and reliable and sensitive biomarkers are still required. The purpose of this present work was to assess in rats the sensitivity of diamine oxidase (DAO) activity, a recently proposed biomarker, to modifications in dietary Cu intake in comparison with other plasma biomarkers of Cu status. We also evaluated the effect of Cu dietary level on Cu and Zn intestinal absorption. Results showed that plasma Cu and plasma caeruloplasmin were significantly decreased at day 8 compared with the control group (7·4 mg Cu/kg diet) while DAO activity was significantly decreased at day 12 of the deficient diet (0·61 mg Cu/kg diet). Cu supplementation (35 mg Cu/kg diet) had no effect on any of the studied biomarkers of Cu status. In Cu-deficient rats plasma Cu and DAO activities were normalized 4 d after return to the control diet while caeruloplasmin was normalized later, at day 11. Apparent absorption values (%) of total Cu or65Cu isotope were significantly increased in the Cu-deficient rats compared with the other groups and similar in the control and the Cu-supplemented groups. The urinary excretion of total Cu or65Cu isotope were increased in the Cu-supplemented group compared with the other two groups. Both apparent absorption and urinary excretion of total Zn or67Zn isotope remained unchanged in the three experimental groups. In conclusion, DAO activity seemed to be less sensitive to Cu deficiency than plasma Cu or caeruloplasmin concentrations. The present study also showed a significant increase in Cu intestinal absorption with dietary Cu restriction but no decrease with Cu supplementation in the rat.

Phosphorus adaptation in rats in absence of vitamin D or parathyroid glands

1980 ◽  
Vol 239 (4) ◽  
pp. G261-G265
Author(s):  
C. F. Cramer ◽  
J. McMillan
Keyword(s):  
Vitamin D ◽  
Urinary Excretion ◽  
Vitamin D Deficiency ◽  
Intestinal Absorption ◽  
Control Diet ◽  
Inorganic Phosphorus ◽  
Parathyroid Glands ◽  
Intestinal Excretion ◽  
Growing Rats ◽  
Pi Deficiency

Growing rats even when vitamin D deficient became adapted to inorganic phosphorus (Pi) deficiency by increasing absorption and minimizing excretion. Feeding low-Pi diet for 3 wk reduced urinary Pi by 80% (P < 0.001), and urinary 32P by 50% (P < 0.001). Low-Pi regimen increased 32p absorption from a 32P-labeled meal by 50% (P < 0.001), even when the animals were vitamin D deficient or thyroparathyroidectomized. The marked increase in retention of 32P in phosphorus-deficient rats could not be accounted for by decreased endogenous intestinal excretion plus increased kidney reabsorption; increased intestinal absorption played a part. 32P absorption was significantly reduced (P < 0.001) by vitamin D deficiency in rats fed either control diet (.6%) Pi or low-Pi diet (0.03%). Endogenous intestinal or urinary excretion of 32P was unaltered by vitamin D deficiency. The evidence supports the hypothesis that there are two mechanisms for phosphorus adaptation: kidney retention not requiring vitamin D, and inreased intestinal absorption of Pi not requiring parathyroids, thyroids, or vitamin D.

Magnesium deficiency protects against Babesia hylomysci and mice become resistant to rechallenge with the parasite regardless of diet fed

Parasitology ◽  
1994 ◽  
Vol 108 (3) ◽  
pp. 245-248 ◽  
Author(s):  
P. Maurois ◽  
P.H. Delcourt ◽  
E. Gueux ◽  
Y. Rayssiguier
Keyword(s):  
Protective Effect ◽  
Magnesium Deficiency ◽  
Control Diet ◽  
Oxidant Stress ◽  
Membrane Properties ◽  
Deficient Diet ◽  
Mg Deficiency ◽  
Deficient Mice

SUMMARYMice were fed diets containing 960 mg (control), 100 mg (moderately Mg deficient) and 30 mg (severely Mg deficient) of Mg/kg. After 20 days, mice were inoculated with Babesia hylomysci (from Dr Wery, Anvers, Belgium). Significant increases in RBC Mg levels were observed following infection. All the control and moderately deficient mice died from infection, whereas the severely Mg-deficient diet protected mice against infection, as shown by a decrease in parasitaemia and mortality. The decrease in RBC Mg, modifications in membrane properties and increased oxidant stress are possible explanations for the protective effect of severe Mg deficiency. When mice were maintained for 2 months after inoculation on a severely Mg-deficient diet and were then switched to a control diet, all survived and had low parasitaemias. After 1 month, these mice were rechallenged with B. hylomysci and 89% survived.

FOOD CONSUMPTION AND RECTAL TEMPERATURE IN RATS DURING THIAMINE DEFICIENCY AND REPLETION

1963 ◽  
Vol 41 (12) ◽  
pp. 2463-2471 ◽  
Author(s):  
M. J. Veen ◽  
G. Russell ◽  
G. H. Beaton
Keyword(s):  
Food Consumption ◽  
Rectal Temperature ◽  
Food Restriction ◽  
Control Diet ◽  
Significant Rise ◽  
Male Rats ◽  
Thiamine Hydrochloride ◽  
Deficient Diet ◽  
Ad Libitum ◽  
Deficient Group

Rectal temperature in male rats fell slowly and gradually from ad libitum and pair-led control levels throughout a thiamine depletion period. During this period, food consumption dropped suddenly and sharply to a minimal level. A single oral dose of 50 μg of thiamine hydrochloride produced, within 4 hours, a significant rise (to less than control levels) in rectal temperature and an increase in food consumption within 24 hours. The increase in temperature was independent of the ingestion of food since diet was withheld during the 4 hours following thiamine administration. Subsequent feeding of control diet (containing thiamine) had not further increased the "4-hour" temperature after 24 hours. With continued feeding of control diet, rectal temperature rose to control levels after 3 days. On subsequent withdrawal of dietary thiamine from the deficient group, temperature and food consumption fell as before. When the animals were again repleted with 50 μg thiamine and deficient diet was continued, temperatures rose to the same level reached after the first thiamine administration. A third deprivation and repletion produced identical results.Food restriction alone, in pair-fed control groups, induced an initial elevation of rectal temperature above ad libitum control levels as temperatures in the deficient group were falling, and an eventual decrease below ad libitum control levels only after prolonged food restriction. It is suggested that the initial fall in body temperature in thiamine-deficient rats is not simply a terminal result of food restriction per se, but may reflect alterations in metabolism due to the deficiency.

Influence of Lysine and NH4Cl Feeding on the Electrolytes of Normal and K-Deficient Rats

1958 ◽  
Vol 193 (3) ◽  
pp. 653-656 ◽  
Author(s):  
Robert E. Eckel ◽  
Charles E. Pope ◽  
James E. C. Norris
Keyword(s):  
Muscle Cell ◽  
Control Diet ◽  
Deficient Diet ◽  
Urine Electrolytes ◽  
K Depletion

Control and K-deficient diets supplemented with lysine HCl and NH4Cl have been fed to rats for 2 or 3 weeks and the tissue and urine electrolytes studied. Lysine when fed in the control diet accumulates in muscle without depletion of muscle K. The lysine accumulation of dietary K depletion is accentuated by lysine feeding and diminished by NH4Cl feeding. Both supplements to the K deficient diet increase urinary K loss. It is concluded that lysine does not compete with K either for entrance into the muscle cell or at the renal level.

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