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.

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

1963 ◽  
Vol 41 (1) ◽  
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.

scholarly journals Hepatic one-carbon metabolism in early folate deficiency in rats

1993 ◽  
Vol 291 (1) ◽  
pp. 145-149 ◽  
Author(s):  
M Balaghi ◽  
D W Horne ◽  
C Wagner
Keyword(s):  
Enzyme Activity ◽  
De Novo ◽  
Folate Deficiency ◽  
Male Rats ◽  
Control Group ◽  
Deficient Diet ◽  
Ad Libitum ◽  
Deficient Group

Glycine N-methyltransferase (GNMT) is inhibited by 5-methyltetrahydrofolate polyglutamate in vitro. It is believed to play a regulatory role in the synthesis de novo of methyl groups. We have used the amino-acid-defined diet of Walzem and Clifford [(1988) J. Nutr. 118, 1089-1096] to determine whether folate deficiency in vivo would affect GNMT activity, as predicted by the studies in vitro. Weanling male rats were fed on the folate-deficient diet or a folate-supplemented diet pair-fed to the deficient group. A third group was fed on the folate-supplemented diet ad libitum. Development of folate deficiency rapidly resulted in decreased levels of S-adenosylmethionine (SAM) and elevation of S-adenosylhomocysteine (SAH). The ratios of SAM to SAH were 1.8, 2.7 and 1.5 in the deficient group for weeks 2, 3 and 4 of the experiment, and the values were 9.7, 7.1 and 8.9 for the pair-fed control group and 10.3, 8.8 and 8.0 for the control group ad libitum fed. The activity of GNMT was significantly higher in the deficient group than in either of the two control groups at each time period. This was not due to increased amounts of GNMT protein, but reflected an increase in specific enzyme activity. Levels of folate in both the cytosol and mitochondria were severely lowered after only 2 weeks on the diet. The distribution of folate coenzymes was also affected by the deficiency, which resulted in a marked increase in the percentage of tetrahydrofolate polyglutamates in both cytosol and mitochondria and a very large decrease in cytosolic 5-methyltetrahydrofolate. The increased GNMT activity is therefore consistent with decreased folate levels and decreased inhibition of enzyme activity.

scholarly journals Butaphosphan Effects on Glucose Metabolism Involve Insulin Signaling and Depends on Nutritional Plan

Nutrients ◽  
2020 ◽  
Vol 12 (6) ◽  
pp. 1856 ◽  
Author(s):  
Maria Amélia Agnes Weiller ◽  
Joao Alveiro Alvarado-Rincón ◽  
Carolina Bespalhok Jacometo ◽  
Carlos Castilho Barros ◽  
Izabel Cristina Custódio de Souza ◽  
...  
Keyword(s):  
Insulin Signaling ◽  
Food Restriction ◽  
Organic Phosphorus ◽  
Control Diet ◽  
Homa Index ◽  
Fat Mobilization ◽  
Reduced Fat ◽  
Epididymal White Adipose Tissue ◽  
Ad Libitum ◽  
Hypercaloric Diet

Butaphosphan is an organic phosphorus compound used in several species for the prevention of rapid catabolic states, however, the mechanism of action remains unclear. This study aimed at determining the effects of butaphosphan on energy metabolism of mice receiving a normal or hypercaloric diet (HCD) and submitted or not to food restriction. Two experiments were conducted: (1) during nine weeks, animals were fed with HCD (n = 28) ad libitum, and at the 10th week, were submitted to food restriction and received butaphosphan (n = 14) or saline injections (n = 14) (twice a day, for seven days) and; (2) during nine weeks, animals were fed with a control diet (n = 14) or HCD (n = 14) ad libitum, and at the 10th week, all animals were submitted to food restriction and received butaphosphan or saline injections (twice a day, for seven days). In food restriction, butaphosphan preserved epididymal white adipose tissue (WAT) mass, increased glucose, NEFA, and the HOMA index. In mice fed HCD and submitted to food restriction, the butaphosphan preserved epididymal WAT mass. Control diet influences on PI3K, GCK, and Irs1 mRNA expression. In conclusion, butaphosphan increased blood glucose and reduced fat mobilization in overweight mice submitted to caloric restriction, and these effects are influenced by diet.

scholarly journals Magnesium and calcium deficiencies additively increase zinc concentrations and metallothionein expression in the rat liver

2012 ◽  
Vol 109 (3) ◽  
pp. 425-432 ◽  
Author(s):  
Megumi Kotani ◽  
Ki Hyun Kim ◽  
Natsumi Ishizaki ◽  
Masayuki Funaba ◽  
Tohru Matsui
Keyword(s):  
Rat Liver ◽  
Control Diet ◽  
Mrna Level ◽  
Male Rats ◽  
Mrna Levels ◽  
Deficient Diet ◽  
Mg Deficiency ◽  
Ca Deficiency ◽  
Zn Concentration ◽  
Dietary Treatments

Mg deficiency increases the concentration of Zn in the liver. We investigated the effect of Mg deficiency on the expression of Zn-regulating factors such as Zn transporters and metallothionein (MT) in the rat liver. Because Ca deficiency alleviates some of the effects of Mg deficiency, we also investigated the interactions associated with Ca and Mg deficiencies. Growing male rats were given a control diet, a Mg-deficient diet, a Ca-deficient diet and a Mg- and Ca-deficient diet for 3 weeks. Mg and Ca deficiencies additively increased the mRNA levels of MT-1 and MT-2, the MT protein concentration and the concentration of Zn in the liver. The hepatic mRNA level of Zip14 increased with Mg deficiency but not with Ca deficiency. The dietary treatments did not affect the mRNA levels of other Zn transporters such as Zip1, Zip5, ZnT1, ZnT5 and ZnT6 in the liver. Ca deficiency was found to decrease the amount of femoral Zn and increase serum Zn concentration. This did not occur in the case of Mg deficiency. These results suggest that Mg deficiency enhances hepatic Zn uptake by the up-regulation of Zip14 expression and increases hepatic Zn concentration, leading to the enhancement of MT expression. Ca deficiency causes a transfer of Zn from the bone to the liver, which increases hepatic Zn concentration and, in turn, up-regulates the expression of MT. Because Mg and Ca deficiencies increase hepatic Zn concentration and increase MT expression by different mechanisms, their effects are additive.

A note on the combined effects of exercise and food restriction on plasma enzyme activities in the rat

1969 ◽  
Vol 47 (4) ◽  
pp. 396-398 ◽  
Author(s):  
J. R. Beaton ◽  
B. Oyster
Keyword(s):  
Food Restriction ◽  
Acute Exercise ◽  
Male Rats ◽  
Elevated Plasma ◽  
Malic Dehydrogenase ◽  
Individual Effects ◽  
Ad Libitum ◽  
The Individual ◽  
Exercise And Training ◽  
And Training

Plasma activities of malic dehydrogenase (MDH) and glutamic–pyruvic transaminase (GPT) were measured in adult male rats made to swim for 1 h either as a single, acute exercise or in repeated exercises (training) in the presence of a 50% food restriction. Food restriction per se elevated MDH and lowered GPT activities. Food-restricted rats responded to both acute exercise and training by an elevated plasma MDH activity. The effect of exercise on plasma MDH activity in these animals was greater than in rats fed ad libitum and was greater than could be accounted for by the summation of the individual effects of training and of food restriction. Plasma GPT activity was not altered by exercise in rats fed ad libitum or in food-restricted animals. It would appear, as suggested previously, that plasma MDH activity may be a useful biochemical criterion of training.

Food restriction increases torpor and improves brown adipose tissue thermogenesis in ob/ob mice

1985 ◽  
Vol 248 (5) ◽  
pp. E531-E539 ◽  
Author(s):  
J. Himms-Hagen
Keyword(s):  
Adipose Tissue ◽  
Body Temperature ◽  
Brown Adipose Tissue ◽  
Rectal Temperature ◽  
Food Restriction ◽  
Normal Body Temperature ◽  
Cold Intolerance ◽  
Brown Adipose ◽  
Brown Adipose Tissue Thermogenesis ◽  
Ad Libitum

Restricting the food intake of the genetically obese (ob/ob) mouse is known to ameliorate its cold intolerance. Cold intolerance of the ob/ob mouse is associated with defective thermogenesis in its brown adipose tissue. The objective of the experiments was to find out whether food restriction could increase the thermogenic function of brown adipose tissue of the ob/ob mouse. Obese and lean mice were fed a restricted amount of chow in one meal per day for 3-7 mo. Both lean and ob/ob mice were torpid (rectal temperature of approximately 32 degrees C) in the early morning and aroused spontaneously to a normal body temperature before the anticipated meal time. Obese mice were also torpid during the dark phase, whereas lean mice were active and had a normal body temperature at this time. Brown adipose tissue was in a thermogenically inactive state (low level of mitochondrial GDP binding) in torpid lean and ob/ob mice but became thermogenically active (increase in mitochondrial GDP binding) during stimulated arousal when body temperature increased by 6-7 degrees C in 15-30 min. Ad libitum-fed ob/ob mice had a normal diurnal rhythm in a rectal temperature that was at a lower level than in lean ad libitum-fed mice. They did not raise their rectal temperatures when stimulated and no activation of brown adipose tissue thermogenesis occurred under these conditions. Food restriction increased the capacity of both lean and ob/ob mice to raise their metabolic rate in response to injection of noradrenaline, indicating an increased capacity for thermogenesis in their brown adipose tissue.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals A Calcium-Deficient Diet in Dams during Gestation Increases Insulin Resistance in Male Offspring

Nutrients ◽  
2018 ◽  
Vol 10 (11) ◽  
pp. 1745 ◽  
Author(s):  
Junji Takaya ◽  
Sohsaku Yamanouchi ◽  
Jiro Kino ◽  
Yuko Tanabe ◽  
Kazunari Kaneko
Keyword(s):  
Insulin Resistance ◽  
Serum Insulin ◽  
Control Diet ◽  
Insulin Resistance Syndrome ◽  
Control Group ◽  
Β Cells ◽  
Deficient Diet ◽  
Ca Deficiency ◽  
Female Wistar Rats ◽  
Deficient Group

Calcium (Ca) plays an important role in the pathogenesis of insulin resistance syndrome. Osteocalcin (OC), a bone formation biomarker, acts directly on β-cells and increases insulin secretion. We determined the effects of Ca deficiency during pregnancy and/or lactation on insulin resistance in offspring. Female Wistar rats consumed either a Ca-deficient or control diet ad libitum from three weeks preconception to 21 days postparturition. Pups were allowed to nurse their original mothers until weaning. The offspring were fed a control diet beginning at weaning and were killed on day 180. Serum carboxylated OC (Gla-OC) and undercarboxylated OC (Glu-OC), insulin and adipokines in offspring were measured. In males, mean levels of insulin, glucose, and HOMA-IR were higher in the Ca-deficient group than in the control group. In addition, ionized Ca (iCa) was inversely associated with serum Glu-OC and adiponectin in males. In females, mean levels of Glu-OC and Gla-OC in the Ca-deficient group were higher than in the control group. In all offspring, serum leptin levels were correlated with serum insulin levels, and inversely correlated with iCa. In conclusion, maternal Ca restriction during pregnancy and/or lactation influences postnatal offspring Ca metabolism and insulin resistance in a sex-specific manner.

Rat muscle structure and metabolism in relation to age and food intake

1982 ◽  
Vol 242 (1) ◽  
pp. R89-R93 ◽  
Author(s):  
R. J. McCarter ◽  
E. J. Masoro ◽  
B. P. Yu
Keyword(s):  
Oxygen Consumption ◽  
Muscle Mass ◽  
Food Restriction ◽  
Fiber Diameter ◽  
Male Rats ◽  
Progressive Loss ◽  
Age Related ◽  
Group A ◽  
Ad Libitum ◽  
Ad Libitum Intake

Age changes in oxygen consumption and the structural composition of the lateral omohyoideus muscle were studied in adult male rats. The rate were either fed ad libitum (group A) or 60% of the ad libitum intake (group R). An age-related loss in muscle mass did not occur even at advanced ages in group A or group R rats. Muscle fiber diameter decreased with age in both groups but a concomitant increase in the number of fibers prevented a change in muscle mass. The muscles of group R rats contained the same number of fibers as those of group A rats at all ages. The muscles of group A rats showed a progressive loss in rate of resting oxygen consumption until 18 mo of age. A similar but less marked loss in oxygen consumption occurred in the muscles of group R rats. These results provide further evidence that life-prolonging food restriction modulates physiological changes associated with the aging process.

Food restriction as a modulator of age-related changes in serum lipids

1980 ◽  
Vol 238 (3) ◽  
pp. E253-E257 ◽  
Author(s):  
G. U. Liepa ◽  
E. J. Masoro ◽  
H. A. Bertrand ◽  
B. P. Yu
Keyword(s):  
Serum Cholesterol ◽  
Food Restriction ◽  
Serum Triglyceride ◽  
Serum Levels ◽  
Male Rats ◽  
Serum Free Fatty Acid ◽  
Young Rats ◽  
Age Related ◽  
Ad Libitum ◽  
Age Related Changes

Fischer 344 male rats were either fed ad libitum or 60% of the ad libitum intake. The restriction of food intake markedly increased the median length of life. Postabsorptive serum cholesterol and phospholipid concentrations increase in the ad libitum-fed rats with increasing age. Life-prolonging food restriction does not influence the serum levels of these lipids in young rats but delays the age-related increase in concentrations. Postabsorptive serum free fatty acid (FFA) concentrations decrease with advancing age in ad libitum-fed rats. Life-prolonging food restriction, while not affecting the serum FFA levels in young rats, delays and possibly partially prevents the age-related decrease in concentration. Food restriction lowers postabsorptive serum triglyceride levels at all ages studied. The data on serum cholesterol, phospholipids, and FFA provide further evidence that food restriction delays age-related changes in the physiological systems of rats. This delay of physiological decline may well retard the occurrence of age-related disease processes, thus prolonging life.

scholarly journals Dietary Pi deprivation in rats affects liver cAMP, glycogen, key steps of gluconeogenesis and glucose production

2000 ◽  
Vol 352 (1) ◽  
pp. 227-232 ◽  
Author(s):  
Wensheng XIE ◽  
T. Luong TRAN ◽  
Diane T. FINEGOOD ◽  
Gérald VAN DE WERVE
Keyword(s):  
Glucose Level ◽  
Glucose Intolerance ◽  
Plasma Glucose ◽  
Phosphoenolpyruvate Carboxykinase ◽  
Control Diet ◽  
Hepatic Glucose Production ◽  
Glucose Production ◽  
Deficient Diet ◽  
Pi Deprivation ◽  
Deficient Group

We previously reported [Xie, Li, Méchin and van de Werve (1999) Biochem. J. 343, 393–396] that dietary phosphate deprivation for 2 days up-regulated both the catalytic subunit and the putative glucose-6-phosphate translocase of the rat liver microsomal glucose-6-phosphatase system, suggesting that increased hepatic glucose production might be responsible for the frequent clinical association of hypophosphataemia and glucose intolerance. We now show that liver cAMP was increased in rats fed with a diet deficient in Pi compared with rats fed with a control diet. Accordingly, in the Pi-deficient group pyruvate kinase was inactivated, the concentration of phosphoenolpyruvate was increased and fructose 2,6-bisphosphate concentration was decreased. Phosphoenolpyruvate carboxykinase activity was marginally increased and glucokinase activity was unchanged by Pi deprivation. The liver glycogen concentration decreased in the Pi-deficient group. In the fed state, plasma glucose concentration was increased and plasma Pi and insulin concentrations were substantially decreased in the Pi-deficient group. All of these changes, except decreased plasma Pi, were cancelled in the overnight fasted Pi-deficient group. In the fasted Pi-deficient group, immediately after a glucose bolus, the plasma glucose level was elevated and the inhibition of endogenous glucose production was decreased. However, this mild glucose intolerance was not sufficient to affect the rate of fall of the glucose level after the glucose bolus. Taken together, these changes are compatible with a stimulation of liver gluconeogenesis and glycogenolysis by the Pi-deficient diet and further indicate that the liver might contribute to impaired glucose homeostasis in Pi-deficient states.

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