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Query: UMLS:C0011849 (
diabetes
)
277,896
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
1. Neither alloxan-
diabetes
nor
starvation
affected the rate of glucose production in hepatocytes incubated with lactate, pyruvate, propionate or fructose as substrates. In contrast, glucose synthesis with either alanine or glutamine was increased nearly 3- and 12-fold respectively, in comparison with that in fed rabbits. 2. The addition of amino-oxyacetate resulted in about a 50% decrease in glucose formation from lactate in hepatocytes isolated from fed, alloxan-diabetic and starved rats, suggesting that both mitochondrial and cytosolic forms of rabbit phosphoenolpyruvate carboxykinase function actively during gluconeogenesis. 3. Alloxan-
diabetes
resulted in about 2-3-fold stimulation of urea production from either amino acid studied or NH4Cl as NH3 donor, whereas
starvation
caused a significant increase in the rate of ureogenesis only in the presence of alanine as the source of NH3. 4. As concluded from changes in the [3-hydroxybutyrate]/[acetoacetate] ratio, in hepatocytes from diabetic animals the mitochondrial redox state was shifted toward oxidation in comparison with that observed in liver cells isolated from fed rabbits.
...
PMID:Effect of alloxan-diabetes on gluconeogenesis and ureogenesis in isolated rabbit liver cells. 74 58
Diabetes
,
starvation
and various hormonal treatments are known to alter drastically carnitine concentrations in the body. Before the mechanisms controlling carnitine metabolism could be determined, it was necessary to establish normal carnitine concentrations in both sexes at different ages. Carnitine was assayed in plasma, liver, heart and skeletal muscle of rats from birth to weaning. The plasma carnitine increased rapidly during the first 2 days after birth. Carnitine in both heart and skeletal muscle increased, whereas liver concentrations declined during the first week of life. A carnitine-free diet containing sufficient precursors for carnitine biosynthesis was fed to weanling rats. Groups of ten male and ten female rats were killed each week for 10 consecutive weeks. Carnitine was determined in plasma, liver, heart, skeletal muscle, urine and epididymis in the male. There was no difference in carnitine concentrations between the sexes at weaning. Plasma, heart and muscle concentrations were higher in adult male rats than in adult females. However, liver carnitine and urinary carnitine concentrations were higher in adult female than in adult male rats. The epididymal carnitine concentration increased very rapidly during 50 to 70 days of age and the differences in carnitine concentrations between the sexes also became apparent during this time. Thus both the age and the sex of the human subject or experimental animal must be considered when investigating carnitine metabolism.
...
PMID:Variation in tissue carnitine concentrations with age and sex in the rat. 74 45
The susceptibility of rats to alloxan undergoes a circadin rhythm. The toxicity rhythm, presumably involving injury to liver, kidney and other sites, pancreatic beta-cells in particular, is demonstrated in pooled data from 370 mature inbred Fischer or Minnesota Sprague-Dawley rats of both sexes kept in light from 06(00) to 18(00) alternating with darkness, some with free access to Purina laboratory chow with tap water at all times and some other rats subjected to one of three
starvation
schedules: 1) a 28-h fast before an intravenous alloxan injection; 2) a 28-h fast, except for a 4-h ad libitum feeding before injection; 3) a 28-h fast, except for a 4-h pre-injection tube-feeding of Nutrament (Mead and Johnson, Evansville, Indiana), 1.5 ml/100 g body weight. Survival time data on an additional 200 inbred Fischer rats reveal, next, that susceptibility to alloxan increases as the
starvation
span is lengthened from 24 to 84 h. The shortening in survival time indicative of this susceptibility increase is nonlinear; a circadian rhythmic change in susceptibility to alloxan is seen as a statistically significant wave-form indicative of the basic (persisting) rhythm, of applied interest as well to students of experimental
diabetes
.
...
PMID:Circadian susceptibility rhythm of the rat to alloxan. 74 84
Twenty-four chronic alcohol abusers hospitalized during a twenty-seven-month period were suspected of having "alcoholic ketoacidosis" because they had ketonuria or ketonemia with little or no glucosuria. Twenty-one had moderate or severe ketosis, with plasma 3-hydroxybutyrate of 5.2 to 22.5 mmol/L. Fifteen of this group were not diabetic, while six were later found to have mild postprandial hyperglycemia without glycosuria. Three patients who had continued to drink until shortly before admission, though at first suspected of having alcoholic ketosis, were found to have predominant lactic acidosis, with minor elevations of plasma 3-hydroxybutyrate. In contrast to previously reported patients with "alcoholic ketoacidosis", severe acidemia was uncommon in this series. Indeed, seven patients were alkalemic, because of coexisting respiratory or metabolic alkalosis. Most patients had eaten poorly for several days (and usually longer) and had allegedly decreased their alcohol intake during that period. That history, and the usual rapid clearing of ketosis simply by treatment with solutions of glucose and NaCl, suggested that acute
starvation
was an important factor in the pathogenesis of this disorder. Four patients were treated with insulin and four with NaHCO3 solutions. In retrospect, the need for either of these treatments was not clear. Two of the twenty-four patients died, one from circulatory failure secondary to hemorrhage and the other from pulmonary edema, but no patient died because of ketoacidosis per se.
Diabetes
1975 Sep
PMID:Alcoholic detosis. 80 36
Using histochemical techniques the glycogen content and the activities of glycogen synthetase (UDPGGT) and phosphorylase were studied in the livers of 106 golden hamsters under following experimental conditions; a)
starvation
of 16, 36, 48, 72, and 96 hours: b) alloxan-
diabetes
.
Starvation
leads to a depletion of liver glycogen during the first 48 hours, which is finally restricted to zone 3 of the liver acinus. After
starvation
of 72 and 96 hours a new glycogen accumulation is demonstrable in the microvasculatory periphery of the acinus (zone 3 and 2). The process of glycogen depletion is characterized in the beginning by a high phosphorylase activity in all zones of the acinus, later only in the forefield of glycogen content. The weak activity of glycogen synthetase is mainly restricted to zone 3. All phases of glycogen depletion are to be found in alloxan diabetic animals, too. Out of 45 hamsters 23 showed an extreme depletion of glycogen; typical for this situation is a weak or absent glycogen synthetase activity in zone 3 and a broad field of phosphorylase activity in zones 1 and 2. The short stimulation by insulin leads to a considerable increase of glycogen synthetase activity at the portally oriented border of the glycogen area and to a shift of the moderate phosphorylase activity of zone 1. Thus the histochemical characteristics of glycogen depletion are: a shift of the reduced glycogen content in direction of the microvasculatory periphery of the liver acinus (zone 3), caused by a high phosphorylase activity in the portal forefield, while glycogen synthetase activity is low in the glycogen area. The histochemical characteristics of glycogen accumulation are: after a short phase of glycogen synthesis in all hepatocytes a moderate phosphorylase activity in zone 1 leads to a mobilization of the portal glycogen deposits and to an increasing accumulation of glycogen in the peripheral part of the acinus. At the portally oriented border of the glycogen area a high synthetase activity leads to a broadening of the glycogen area in direction of the portal branches. At the end of this process the "normal" pattern of the liver acinus occurs: all hepatocytes are filled with glycogen, the glycogen enzymes are restricted to the periportal border of zone 1.
...
PMID:Dynamics of liver glycogen: the topochemistry of glycogen synthesis, glycogen content and glycogenolysis under the experimental conditions of glycogen accumulation and depletion. 81 13
Four adolescents or young adults with the Prader-Willi syndrome (hypotonia, mental retardation, hypogonadism and obesity) received a protein-sparing modified fast consisting of 1.5 g of meat protein per kilogram of ideal body weight and meeting vitamin, mineral and fluid requirements. Evaluation of nitrogen and energy metabolism revealed the development of
starvation
ketosis and a positive nitrogen balance. Serial whole-body potassium measurements in two patients confirmed preservation of lean tissue despite continuing loss of weight. Clinical
diabetes mellitus
in two subjects was rapidly ameliorated by the regimen. Short-term weight loss greater than 18 kg occurred in three of the four subjects, and reduced weight persisted during observation periods of 26 to 44 months. This degree of outpatient diet adherence by mentally deficient subjects, who do not normally experience satiety, suggests that hunger is eliminated or at least reduced by modified, protein-sparing fasting.
...
PMID:Metabolic aspects of a protein-sparing modified fast in the dietary management of Prader-Willi obesity. 84 Feb 78
The influence of low carbohydrate (CHO) diets,
starvation
, and high CHO diets on glucose tolerance tests (GTT) and plasma insulin response of men with chemical
diabetes
was studied. The GTT and insulin responses of these seven lean diabetic men were unchanged when the carbohydrate content of the diet was reduced from 44 to 20% of calories. After a 48-hr fast a significant deterioration of the GTT was observed in these diabetic men but the percentage change was identical to that reported previously for normal men. Thus these studies indicate that changes in glucose mtes are quite similar to those reported previously for normal men. The fasting plasma glucose values of seven lean and four obese men with chemical
diabetes
were significantly lower after one week on a 75% CHO diet than values on a 44% CHO diet. The 75% CHO diet also was accompanied by slight improvements in the oral and intravenous GTT and by slightly lower plasma insulin responses. The improvement in glucose metabolism on high CHO diets appears to results from increased insulin sensitivity. Serum triglyceride values were approximately 55% higher on the 75% CHO diet than values on the 44% CHO diet for the 11 men but these differences were not statistically significant. These studies support previous observations and suggest that high CHO diets may be beneficial in the management of certain diabetic patients. However, further studies are required to determine the long-term effects of high CHO diets containing natural foods on the glucose and lipid metabolism of diabetic patients.
...
PMID:Effect of carbohydrate restriction and high carbohydrates diets on men with chemical diabetes. 84 91
Higher omega-oxidation activities in the diabetic mammal and the starved one suggest that omega-oxidation mechanism plays an important role under these conditions. Dicarboxylic acid that is the final product of omega-oxidation can be metabolized further by beta-oxidation, subsequently, formation of succinyl-CoA and short-chain dicarboxylic acid might be increased in the liver. The physiological significance of omega-oxidation might consist in supplying the substrate of TCA cycle for utilization of acetyl-CoA and excreting the short-chain dicarboxylate in urine resulting in the decrease of ketone bodies in the blood, especially in
diabetes
and
starvation
. On the bases of these information, it is important to investigate the metabolism of dicarboxylic acids. Generally, fatty acids must be activated before they enter the metabolic pathway. By in vitro studies with rat liver homogenate, we have recently demonstrated that octadecaned-ioic acid must be activated by ATP-Mg2+ and CoA as monocarboxylic acid is. However, it has not been studied to compare the activity of acyl-CoA synthetase on mono and dicarboxylic acid. So, in this report, we assayed the activity of acyl-CoA synthetase in beef liver preparations using palmitic or hexadecanedioic acid (C1;16) as substrate. The results are as follows 1) Activation capacity of the supernatant of sonicated mitochondria was less than that of sonicated microsome for either palmitate or hexadecanedioate. 2) Activation capacity for hexadecanedioate was less than that for palmitate in both supernatant of sonicated mitochondria and that of sonicated microsome. 3) In our experiment, it might be suggested that the subcellular distribution of hexadecanedioate activation is almost identical with that of palmitate activation.
...
PMID:[Acyl-CoA synthetase activity of long-chain mono and dicarboxylic acid in beef liver preparations (author's transl)]. 94 21
1. The regulation of the synthesis of phosphoenolpyruvate carboxykinase (GTP) (EC 4.1.1.32) in epididymal adipose tissue, liver and kidney in vivo was studied immunochemically. 2. Phosphoenolpyruvate carboxykinase (GTP) synthesis in adipose tissue is increased by
starvation
,
diabetes
and noradrenaline, and decreased by re-feeding and insulin. These changes were also seen in adrenalectomized rats and are qualitatively similar to those observed for the liver enzyme. This indicates the involvement of cyclic AMP as an inducer and insulin as a de-inducer in the regulation of phosphoenolpyruvate carboxykinase (GTP) in both tissues. (Induction and de-induction are defined as selective increase and decrease respectively in the rate of enzyme synthesis, regardless of the mechanism involved.)3. Adrenalectomy had little effect on phosphoenolpyruvate carboxykinase (GTP) synthesis in liver and kidney, but increased the synthesis rate of the adipose-tissue enzyme.
Starvation
and adrenalectomy had additive effects in increasing the synthesis rate of adipose-tissue phosphoenolpyruvate carboxykinase (GTP). In adrenalectomized diabetic rats glucocorticoids increased phosphoenolpyruvate carboxykinase (GTP) synthesis in liver and kidney while decreasing enzyme synthesis in adipose tissue. De-induction of adipose tissue phosphoenolpyruvate carboxykinase (GTP) is therefore regulated independently by glucocorticoids and insulin. 4. Although liver, kidney and adipose-tissue phosphoenolpyruvate carboxykinases (GTP) are seemingly identical, there is an apparent tissue-specific differentiation in regulatory systems for the enzyme.
...
PMID:Regulation of phosphoenolpyruvate carboxykinase (GTP) in adipose tissue in vivo by glucocorticoids and insulin. 96 85
Glucose, apart from its acute insulin-releasing effect, exerts a time-dependent potentiating action on subsequent stimulations of the pancreas. The influence of a 24-hour
starvation
on these two actions of glucose was studied with the completely isolated, perfused rat pancreas preparation.
Starvation
had no effect on the time kinetics of the insulin response, but the magnitudes of the early and late insulin-secretion phases were reduced to similar extents. It was demonstrated by using a wide glucose concentration range that the maximal insulin response is not significantly modified by
starvation
. In contrast, both the threshold of stimulation by and the Km for glucose were higher in the pancrease from fasted rats. Thus,
starvation
reduces the sensitivity of the islet for the insulin-releasing action of glucose. When the stimulatory concentrations of glucose were preceded for 40 minutes by the perfusion of 8.3 mM instead of the basal, 4.4 mM glucose, insulin secretion from the pancreas of fed animals was not modified. In contrast, raising the glucose concentration of the equilibrium period to 8.3 mM potentiated markedly the insulin response to subsequent stimulations in the pancreas from fasted rats. This potentiation expressed itself as increase in the maximal response: the Km for glucose was not reduced. Thus a 40-minute pretreatment with 8.3 mM glucose does not correct the diminished sensitivity induced by a 24-hour
starvation
. It is concluded that in
starvation
(1) the sensitivity for glucose of the mechanisms that initiate insulin release is diminished; (2) the sensitivity of the pancreas for the potentiation-inducing action of glucose is augumented. (3) In both respects, the insulin response of fasted rats is similar to that of mildly diabetic subjects. These and other findings suggest that the effect of glucose in initiation of insulin release and on generation of a state of potentiation in the islet are mediated by different mechanisms.
Diabetes
1976 Oct
PMID:Potentiation of glucose-induced insulin release by glucose in the isolated pancreas of fed and fasted rats. 97 3
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