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Biomedical subjects

N Baker

Publications and source records attributed to N Baker.

At least 109 records · Page 6Linked to original sources
PubMed1977

Measurement of glucose recycling and liver glycogen synthesis in mice using doubly labeled substrates.

Tracer experiments have been carried out using gorging and nibbling mice to study several related aspects of carbohydrate metabolism: 1) inhibition of gluconeogenesis shortly after animals ingest a glucose-rich meal; 2) the extent to which dietary glucose carbon is recycled by way of 3C compounds after dietary glucose is absorbed; and 3) recycling of glucose by exchange between free and a hypothetical, "bound" glucose pool. Fasted, gorging mice were allowed to eat 120 mg [U-14C,6-T]glucose (58% glucose diet) in 4 min. Plasma glucose-C specific activity rapidly reached that of the dietary glucose-C. Superficially, this suggested nearly complete inhibition of hepatic gluconeogenesis. However, plasma [6-T]glucose, glycogen-[14C, 3H]glucose analyses, and [14C]-glycerol conversion to glucose showed that hepatic gluconeogenesis continued during alimentary hyperglycemia. Half of liver glycogen seemed to be formed from a hepatic G-6-P pool that was never labeled. Indirect kinetic evidence of a large, bound exchangeable glucose pool was presented. Since no direct evidence of such a pool has been obtained, the possibility is raised that a serious artifact of the tracer technique exists or else some unconventional model of carbohydrate metabolism is required to explain our data.

Animals↗
PubMed1976

Contribution of intermuscular fat to lipogenesis from dietary glucose carbon in mice.

We assessed the contribution of various tissues to the synthesis of fat from glucose carbon in mice during rapid lipogenic activation induced by a glucose test meal. Nibbling and gorging mice were maintained on a 58% glucose, fat-free diet. The mice were fasted 22 h and refed 5-10 muCi [U-14C]glucose (120 mg/20 g body weight) either by gastric intubation or as a test meal (58% glucose diet). The muscular carcass in both nibblers an gorgers contained more than 75% of the total radioactivity in the fatty acids derived from glucose; liver and epididymal fat pad accounted for only a small percentage. Mort than half the carcass activity was in the "muscular" tissue as neutral lipid acids. We could isolate a discrete fat body in the popliteal region of the leg muscle ("muscle fat", "intermuscular fat"). The popliteal fat converted glucose carbon to fatty acids an order of magnitude faster, per unit weight, than the epididymal fat pad or skeletal muscle. The fatty acid moiety of the triacylglycerols had the major portion of the label in the popliteal fat 2 and 6 h after ingestion of the glucose test meals. The diacylglycerol pool was active at 2 h and its activity faded at 6 h implicating its intermediary role in lipid metabolism similar to published findings in epididymal fat pad. These results indicate that fat cells associated with the muscular carcass may play a major role in the de novo synthesis of fat from dietary carbohydrate in mice.

Adipose Tissue↗
PubMed1976

Net changes in intermuscular fat before and during rapid lipogenic activation in mice.

We have attempted to measure net changes in lipid content in a discrete "intermuscular" fat pad during rapid lipogenic activation that occurs after a previously fasted mouse nibbles a glucose-rich test meal for several minutes. The popliteal fat pad was chosen for the study since it has been shown to be about an order of magnitude more active than the epididymal fat pad in the synthesis of fatty acids from glucose carbon in fasted-refed mice. We found a highly reproducible net loss in the popliteal fat pad's weight and lipid content during fasting. Net deposition of lipid occurred when 24-h fasted mice were allowed to eat a fat-free, 58% glucose diet for several minutes. In two out of three experiments lipid repletion was complete after one brief period of nibbling. Significant decreases in the net amounts of each majority fatty acid, 16:0, 16: 1, 18:1 and 18:2, were found to occur in the popliteal fat pad during a 24-h fast. After nibbling their test meal for several minutes, previously fasted mice restored their major essential fatty acid, linoleic acid, to the original fed level within 2 h, even though total lipid repletion was incomplete. Highly significant net increases in each major non-essential fatty acid were also found after brief ingestion of the test meal; however, in one experiment (incomplete repletion) only about half of the depleted fatty acids was restored. When two successive glucose test meals were eaten (2-h interval), popliteal fat converted glucose carbon to fatty acids more than twice as fast after the second feeding as after the first. However, no significant additional increment either in tissue weight or in total lipid fatty acids was found after the second test meal. Based on these findings, the possible significance of intermuscular fat in the utilization and deposition of fat is discussed.

Adipose Tissue↗
PubMed1976

Blood sampling techniques for studying rapidly turning over metabolic fuels in mice.

Experiments were carried out in control and Ehrlich ascites carcinomatous mice to determine whether orbital venous sinus blood could be used to reflect blood in the systemic circulation (decapitation blood) in the case of a rapidly turning over metabolic fuel such as free fatty acids. The early time course of intravenously injected, labeled free fatty acids was measured using (9, 10-(3)H) palmitic acid and (1-(14)C) linoleate complexed to mouse serum. No significant differences between decapitation and orbital sinus blood were found at early times in either group of mice. The orbital sinus clearly contains blood that is not stagnant and is replaced so rapidly that it is suitable for studying very rapidly turning over, circulating metabolites.

Animals↗
PubMed1976

The significance of electrode surface area and stimulating thresholds in permanent cardiac pacing.

This paper reports a long-term clinical study of evolving chronic thresholds of cardiac stimulation in patients with implanted pacemakers and two types of permanent prevenous unipolar pacing leads. A comprehensive collection of threshold measurements is presented and analyzed. These data were accumulated over a period of more than 4 years by measuring stimulation thresholds at each of five stimulus pulse durations ranging from 0.5 to 2.5 msec. Measurements were made at initial implantation and at first (21 month) and second (42 month) reimplantations.

Electric Stimulation↗
PubMed1976

Equally rapid activation of lipogenesis in nibbling and gorging mice.

Minimal average rates of exogenous glucose-C-conversion to whole body, total lipid fatty acids were measured in nibbling and gorging mice. Gorgers trained to eat 1 meal/day (8-10 am) were fasted 22-24 hr and given [14C]glucose with pure glucose, 30% glucose in water, or a 58% glucose, fat-free diet. Conversion of glucose-C to total lipid fatty acids increased from 0.6 (fasted) to approximately 20 mug/min/20 g body weight during 40 min after glucose feeding using each test meal. Dietary amino acids were not required for activation of lipogenesis in gorgers. Exogenous glucose-C was incorporated into fatty acids as fast in nibbling mice as in gorgers. This was true after varying all of the following conditions: training period, number of meals gorged, previous fasting time, and diet composition. The total rate of fatty acid synthesis from body glucose-C during absorption of a glucose load was also estimated in absorption of a glucose load was also estimated in previously fasted nibbling and gorging mice. These estimates were based on composite, serial measurement of both plasma glucose specific activities and 14C-labeled fatty acids. The total rate of fatty acid synthesis from both exogenous and endogenous glucose-C was only 15% higher than the rate from exogenous glucose-C between 10 and 40 min. No significant differences between nibblers and gorgers were found.

Animals↗
PubMed1975

Tumor extracellular triglycerides in mice during growth of Ehrlich ascites carcinoma.

Our earlier work with Swiss-Webster mice has shown that most of the lipid in Ehrlich ascites tumor extracellular fluid is in the form of free fatty acids. This finding is in direct contradiction to earlier and subsequent reports from another laboratory that has found free fatty acids to be a very minor component and triglycerides to be the major lipid of Ehrlich ascites tumor extracellular fluid. In light of these contradictory reports, we have carried out a study patterned after that of other workers, but using our Swiss-Webster mice. As predicted from our earlier study, we have found very little triglyceride in Ehrlich ascites tumor extracellular fluid. Although we could demonstrate a significant, transient hypertriglyceridemia during tumor growth, maximum plasma triglyceride concentrations were an order of magnitude lower than those reported by other workers. In addition, and again in contrast to other reports, we found that plasma triglyceride and tumor extracellular fluid triglyceride levels in tumorous mice fell significantly with fasting. Thus, interesting differences in triglyceride metabolism between mouse and/or tumor strains seem to exist. Our present findings suggest, but do not prove, that triglycerides in the tumor extracellular fluid probably are not a major source of the rapidly turning over, tumor extracellular fluid free fatty acid in our mice.

Animals↗
PubMed1975

Novel interference in thiobarbituric acid assay for lipid peroxidation.

The thiobarbituric acid test for lipid peroxidation, when applied to a mixture of acetaldehyde and sucrose, produces a 532 nm aborbing chromogen which is indistinguishable from that formed by malonaldehyde and thiobarbituric acid. Unless special procedures are adopted to correct for this effect, the combined action of acetaldehyde and sucrose interferes seriously with the assay of lipid peroxidation reactions, notably those implicated in alcohol-induced liver injuries. However, this unusual thiobarbituric acid effect also can be used as a sensitive method for the detection of acetaldehyde.

Acetaldehyde↗
PubMed1974

Flux of free fatty acids among host tissues, ascites fluid, and Ehrlich ascites carcinoma cells.

The role of plasma free fatty acids (FFA) in the transport of fatty acids from host tissues to Ehrlich ascites carcinoma in mice was studied. [9,10-(3)H] Palmitate complexed to mouse serum (albumin) was injected either intraperitoneally or intravenously into unanesthetized tumor-bearing mice. The incorporation of radioactivity into tumor extracellular fluid FFA, tumor cell FFA, neutral lipid, phospholipid, water-soluble material in cells and fluid, plasma FFA, host carcass total lipid fatty acids, and water-soluble (i.e., nonlipid) material was measured. In addition, the quantity of fatty acid in each of the above lipid fractions was determined. The data were analyzed by multicompartmental analysis (SAAM) using a digital computer, and fractional rate constants of FA movement within and out of the host-tumor system were calculated. These rate constants and pool size measurements were used to estimate the corresponding fluxes. Although FFA in the tumor's extracellular fluid were replaced rapidly, almost none of the newly formed fluid FFA was derived from plasma FFA. Moreover, the transfer of FFA from the tumor extracellular fluid FFA to plasma FFA was virtually negligible. We suggest that the net amount of FFA required to replace the fluid FFA utilized for tumor energy and growth may be derived from direct transfer of FFA from host tissues to the ascitic fluid and that plasma FFA is not an intermediate in this transport process. The transport of FFA from the host to tumor cell lipids through the tumor extracellular fluid was about 26-fold greater than that required to account for net lipid accumulation during growth.

Animals↗
PubMed1973

Lipogenic activation after nibbling and gorging in mice.

Lipogenic activation was studied in mice that had been restricted to a single large meal once a day rather than being allowed to eat at frequent intervals throughout the night. Mice were injected intravenously with [U-(14)C]glucose, and the flux of glucose C to total lipid fatty acids (TLFA) and to all "end products" was estimated from serial plasma glucose specific activities and measurements of incorporation of (14)C into TLFA of hepatic and extrahepatic tissues. Tracer studies were carried out in mice fasted for 1 day and at various times after the mice ate one or two small test meals or a single large test meal. Test meals consisted of a fat-free, 58% glucose diet. The flux of glucose C to TLFA increased by an order of magnitude within an hour after mice nibbled a test meal for several minutes. After ingestion of two small test meals or a single large test meal, the flux of glucose C to TLFA increased from a fasting rate of 0.5 to 35 and 87 micro g of glucose C/min/20 g body wt, respectively. Although trained meal eaters are thought to have abnormally increased lipogenesis, their lipogenic response to a single test meal was the same as that previously reported for untrained nibbling mice. Most of the newly synthesized fatty acids were found in extrahepatic tissues. Ingestion of a first test meal completely prevented the expected hyperglycemic response following ingestion of a second test meal even though the latter contained over 10 times more glucose than that in the total body glucose pool.

Acetates↗
PubMed1973

Specific role of glucose in rapid lipogenic activation in vivo.

Lipogenesis from glucose C was previously found to be rapidly activated as soon as mice nibbled a fat-free, glucose-rich diet. We have studied here whether such rapid activation is a specific effect of dietary glucose. The flux of endogenous glucose C to total lipid fatty acids (TLFA) in mice fasted for 1 day was compared with the minimal average flux of exogenous dietary glucose to TLFA during a 40-min period after the ingestion of various glucose-rich test meals by previously fasted mice. The fasted mice were injected intravenously with [U-(14)C]glucose, and the flux of glucose C to TLFA and to all "end products" was estimated from serial plasma glucose specific activity measurements and (14)C incorporation into TLFA 30 min after (14)C injection. Only 0.6 to 0.8 micro g of glucose C/min/20 g body wt was converted to TLFA, whereas 208 +/- 16 micro g of glucose C/min/20 g body wt was converted to all "end products" in the fasted animals. Previously fasted mice were fed [(14)C]glucose in small test meals as a neat solid, as a 30% aqueous solution, or as a fat-free, 58% glucose diet. During the next 40 min, the average flux of glucose C into TLFA increased at least 50- to 60-fold, regardless of the form in which glucose was fed; however, when glucose was fed as part of a complete fat-free diet, glucose was utilized at a much lower plasma glucose level than in mice fed either pure solid glucose or an aqueous glucose solution. Rapid activation of lipogenesis from glucose requires only glucose as a dietary constituent.

Animals↗