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Biomedical subjects

N K Edens

Publications and source records attributed to N K Edens.

14 recordsLinked to original sources
PubMed1999

Adrenalectomy reduces adiposity by decreasing food efficiency, not direct effects on white adipose tissue.

OBJECTIVE: This study was conducted to establish the effects of adrenalectomy (ADX) on adipose tissue metabolism in male Sprague-Dawley rats fed a standard chow diet. RESEARCH METHODS AND PROCEDURES: The effects of adrenalectomy on adipose cell size, lipoprotein lipase activity, and basal and insulin-stimulated glucose conversion to lipid and lipolysis were measured. RESULTS: ADX decreased body weight gain during the post-operative period in the absence of changes in food intake; feed efficiency was decreased significantly. ADX decreased adipocyte size by 30%. ADX increased adipocyte response to the effect of submaximal concentrations of insulin on lipid synthesis and lipolysis. ADX decreased maximally insulin-stimulated lipid synthesis, but this effect was accounted for by decreased adipocyte size. In contrast, ADX had no effect on maximally insulin-inhibited lipolysis. ADX did not affect heparin-releasable LPL. The small effect of ADX on residual extractable adipose tissue LPL activity was accounted for by decreased fat cell size. DISCUSSION: ADX decreased adiposity in the absence of changes in food intake, lipoprotein lipase activity, and adipocyte lipid metabolism. The effect is best attributed to decreased feed efficiency.

Adipocytes↗
PubMed1993

Lipolysis in intraabdominal adipose tissues of obese women and men.

Intraabdominal fat in humans is located in two major depots, the omental and mesenteric. We compared basal and stimulated lipolysis in adipose tissue from these two depots and the subcutaneous abdominal depot of obese women and men. Omental fat cells of women are smaller and have lower rates of basal lipolysis than in men. Basal lipolysis rates are significantly higher in subcutaneous than intraabdominal adipose tissues of both genders. In men, the incremental lipolytic response to norepinephrine is significantly greater in both intraabdominal fat depots than in the subcutaneous fat, while in women the response of the mesenteric is lower than the omental. In women, but not men, responsiveness to the beta agonist isoproterenol is also increased in omental tissue. Thus, in women, omental and mesenteric adipose tissues show distinctly different metabolic properties which may moderate the impact of intraabdominal obesity.

Abdomen↗
PubMed1993

In vitro lipid synthesis in human adipose tissue from three abdominal sites.

The association between abdominal deposition of adipose tissue and morbidities accompanying obesity may be related to high rates of free fatty acid release from enlarged intra-abdominal stores. To investigate cellular mechanisms that might contribute to enlargement of intra-abdominal adipocytes, lipolysis, triacylglycerol (TG), and diacylglycerol (DG) synthesis from [14C]glucose was measured in abdominal subcutaneous, omental, and mesenteric adipose tissue from severely obese women and men. Subcutaneous adipose tissue from women showed the highest rates of TG synthesis compared with the intra-abdominal site, or any site in men. isoproterenol stimulated TG synthesis more in intra-abdominal than subcutaneous adipose tissue. In the basal state, intra-abdominal adipose tissue from both men and women showed rates of [14C]DG accumulation approximately 50% total [14C]acylglyceride accumulation, whereas, in subcutaneous adipose tissue, [14C]DG accumulation was approximately 25% of total. Basal lipolysis was lower in intra-abdominal than subcutaneous adipocytes. Stimulation of lipolysis reduced [14C]DG accumulation more in intra-abdominal than subcutaneous adipose tissue. Low rates of acylglyceride synthesis in intra-abdominal adipocytes may prevent accumulation of large intra-abdominal fat stores in women.

Abdomen↗
PubMed1990

Lipolytic effects on diacylglycerol accumulation in human adipose tissue in vitro.

When fragments of rat or human adipose tissue, or isolated adipocytes, are incubated with [14C]glucose in vitro, [14C]diacylglycerol accumulates rapidly: it comprises 20-50% of newly synthesized (14C-labeled) acylglycerols, compared to less than 1% diacylglycerol accumulated in the bulk lipid store in vivo. The experiments reported in this study were performed to test the possibility that agents that influence the rate of lipolysis might differentially affect the accumulation of di- and triacylglycerol in human adipose tissue, and perhaps account for the discrepancy between the early labeling and the later accumulation of diacyglycerol. Fragments of gluteal subcutaneous adipose tissue obtained from obese men and women were incubated with isoproterenol, epinephrine plus yohimbine, adenosine deaminase, or dibutyryl 3',5'-cyclic adenosine monophosphate to stimulate lipolysis. Tissue fragments were also incubated with clonidine, adenosine, or insulin to inhibit lipolysis. No agent had any effect on the rate of accumulation of newly synthesized triacylglycerol. The effects of these agents on the rate of lipolysis were negatively correlated with their effects on accumulation of newly synthesized diacylglycerol. Newly synthesized diacylglycerol may be preferentially hydrolyzed by hormone sensitive lipase. This increased susceptibility to lipolytic stimulation, compared to newly synthesized triacylglycerol, may account for the minute accumulation of diacylglycerol in adipose tissue in vivo.

Adenosine↗
PubMed1990

Mechanism of free fatty acid re-esterification in human adipocytes in vitro.

Within adipose tissue, free fatty acids liberated by lipolysis may be re-esterified into newly synthesized triacylglycerol. We hypothesized that re-esterification may occur via an extracellular route, such that free fatty acids arising from lipolysis must leave the adipocyte and be taken up again before they can be re-esterified. We simultaneously measured rates of lipolysis, acylglycerol synthesis, and free fatty acid re-esterification in human adipose tissue and isolated adipocytes in vitro, utilizing a dual-isotopic technique. We manipulated incubations to increase mixing of released free fatty acids with the incubation medium. Such manipulations should decrease the probability that released free fatty acids would be taken up and re-esterified. We found that re-esterification was decreased in isolated adipocytes compared to fragments of tissue, in shaken compared to unshaken incubations, and in low adipocyte concentrations compared to high adipocyte concentrations. Rates of acylglycerol synthesis and lipolysis were unaltered by these manipulations, indicating that changes in free fatty acid re-esterification are not secondary to effects on these processes. The results are consistent with an extracellular route for free fatty acid re-esterification. Such a mechanism suggests that adipose tissue blood flow may play an important role in the regulation of free fatty acid release from adipose tissue.

Adipose Tissue↗
PubMed1989

The fat cell.

Investigations of how fat cells develop, store, and release energy, and what role they play in energy metabolism are presented. The importance of adipose tissue in the pathogenesis of obesity is considered.

Adipose Tissue↗
PubMed1988

Satiating effect of fat in diabetic rats: gastrointestinal and postabsorptive factors.

Streptozotocin-diabetic rats decrease food intake more than normal animals in response to a fat test meal. To determine the physiological basis of this differential response, we examined the effects of an ingested corn oil meal on food intake, gastrointestinal fill, and plasma triglycerides, glycerol, and ketone bodies. Hyperphagic diabetic rats decreased intake of a high-carbohydrate, low-fat stock diet starting 2-4 h after the fat meal, whereas normal rats did not. Gastric emptying was accelerated and intestinal mass and contents were increased in diabetic rats. The fat meal reduced gastric emptying and increased stomach contents in diabetic and normal rats starting within 2 h of ingestion. Intestinal fill decreased in diabetic animals after the oil meal. Triglycerides and glycerol increased transiently after fat ingestion in normal and diabetic rats, whereas ketone body concentrations rose only in diabetic rats starting 1-3 h after fat ingestion. The results indicate that the differential effect of a fat meal on food intake in normal and diabetic rats is related to differences in the postabsorptive metabolism of the ingested fat rather than to effects of fat feeding on gastrointestinal fill or clearance.

Animals↗
PubMed1986

The effects of varying energy and nitrogen intake on nitrogen balance, body composition, and metabolic rate.

Body protein content (as measured by N balance) is normally regulated at a constant level, but is influenced by the level of both energy and N intake. Energy and N act synergistically on N balance. Not all forms of energy are equally effective in maintaining zero N balance; approximately 500 kcal of carbohydrate are required daily by the brain, and this minimum amount of dietary carbohydrate cannot be replaced by fat without loss of body N. Acute illness is accompanied by a catabolic state and an increase in the minimum N intake required for zero N balance. Nutritional depletion induces a metabolic state similar to that typical of growing organisms, in that N can be retained at zero energy balance. BMR includes essential thermogenesis and facultative thermogenesis. In addition, food has a specific dynamic action; it increases metabolic rate. Nutrient-induced increases in metabolic rate are exaggerated in acutely ill patients, such that large amounts of IV glucose may constitute a metabolic stress when given to patients. Equivalent N sparing can be obtained when as much as half of the glucose calories are replaced by fat calories. N balance is an incomplete index of nutritional status, and important information may be gained from measurements of body composition of acutely ill patients; in particular, the degree of expansion of ECW may predict outcome.

Acute Disease↗
PubMed1985

Food intake in diabetic rats: isolation of primary metabolic effects of fat feeding.

The effects of varying dietary fat content on food intake and metabolism in streptozotocin-diabetic rats were examined. The metabolic consequences of fat feeding were separated from the marked adjustments in voluntary food consumption that occur when diabetic rats are fed diets containing different amounts of fat by feeding rats a fixed ration of food in which either fats or carbohydrates were reduced by equicaloric amounts, or in which only the concentration of fat, but not other dietary nutrients, was varied systematically. Resulting changes in metabolism and subsequent ad libitum food intake on refeeding were then measured. Rats did not increase their food intake after a prior reduction in carbohydrate consumption but did so after an equicaloric reduction in fat consumption. Urinary glucose excretion during rationing was a function of carbohydrate consumption and was not predictive of changes in food intake during refeeding. The more fat that rats consumed during rationing, the higher their levels of plasma triglycerides and ketone bodies were at the time of refeeding and the less they ate when allowed to eat ad libitum. The orderly changes in food consumption and in plasma triglycerides and ketones observed with variations in fat intake suggest that the effects of fat feeding on food intake in diabetic rats are mediated through the oxidation of ingested fat.

Animals↗
PubMed1984

Response of normal and diabetic rats to increasing dietary medium-chain triglyceride content.

Replacing dietary long-chain triglycerides (LCT) with medium-chain triglycerides (MCT) has not previously been shown to produce reliable changes in caloric intake. However, diabetic rats are particularly sensitive to changes in the fat content of their diet, and thus were used for comparison to normal rats in the studies reported below. Rats were fed synthetic diets that contained either corn oil or MCT. Food intake and plasma metabolic fuels were measured as the fat content of the diet was increased from 5 to 15 to 25%. Both normal and diabetic MCT-fed rats adjusted their caloric intake more quickly than LCT-fed rats as the fat content of the diet was increased. The relative preference of MCT- and LCT-fed rats for high and low concentrations of dietary fat was assessed. It was found that both normal and diabetic LCT-fed rats preferred high dietary fat, whereas MCT-fed rats did not. In normal rats, plasma triglycerides and glycerol were decreased and plasma ketones increased by MCT feeding. In diabetic rats, the only effect of MCT feeding was to decrease plasma glycerol and triglycerides. The relative importance of hedonic and metabolic feedback to the rapid caloric regulation of MCT-fed rats is discussed.

Animals↗
PubMed1983

Differential effects of medium- and long-chain triglycerides on food intake of normal and diabetic rats.

Three experiments were performed to examine the effect of ingestion of medium- (MCT) and long-chain (LCT) triglyceride oils at the beginning of the normal feeding period on subsequent food intake of normal and diabetic rats. In the first experiment, diabetic rats reduced food intake more than normal animals in the first 6 hr after ingestion of 2.0 ml of MCT or LCT oil. In the second experiment, diabetic rats reduced food intake to a similar extent by 6 hr after ingestion of 1.5 ml of MCT or LCT oil, but the time course of this effect depended on the oil ingested. Ingestion of MCT oil produced a decrease in food intake within 2 hr, whereas ingestion of LCT oil reduced food intake 2-4 hr later. In the third experiment, a direct comparison was made of the differential time course of food intake suppression by MCT or LCT oil in both normal and diabetic rats. Diabetic rats decreased food intake after ingestion of 1.5 ml MCT or LCT oil, whereas normal rats did not. Again, in diabetic rats, ingestion of MCT oil produced a more rapid reduction in food intake than ingestion of LCT oil. It is proposed that the more pronounced reduction in food intake of diabetic rats after oil ingestion is due to a greater degree of hepatic oxidation of ingested fat, whereas the differential effect of MCT and LCT oil ingestion in diabetic rats is due to a differential rate of delivery of the ingested lipid substrate to the liver.

Animals↗
PubMed1983

Effects of estradiol on tissue distribution of newly-synthesized fatty acids in rats and hamsters.

Estradiol treatment decreases body weight and adiposity in ovariectomized (OVX) rats and hamsters partly by increasing energy expenditure. Other manipulations which increase energy expenditure (e.g., cold exposure or overfeeding) enhance thermogenesis in brown adipose tissue (BAT) and stimulate BAT fatty acid synthesis/uptake. We examined the effect of estradiol treatment on the in vivo distribution of newly-synthesized fatty acids in OVX rats and hamsters. In both species estradiol treatment increased BAT fatty acid synthesis/uptake (incorporation of tritium from (3H)2O into lipid), consistent with the possibility that enhanced thermogenesis in BAT may contribute to estradiol-induced energy expenditure. Estradiol treatment increased BAT lipoprotein lipase (LPL) activity in hamsters, but not in rats. Thus, hamsters may utilize fatty acids synthesized in other tissues as a fuel for BAT thermogenesis, whereas rats may rely more on in situ lipogenesis. Estradiol-induced decreases in carcass adiposity (white adipose tissue mass) may be accomplished by different means in rats and hamsters. Estradiol treatment reduced white adipose tissue LPL activity and fatty acid synthesis/uptake in rats, but not in hamsters. While there are some species differences in the effects of estradiol on lipid metabolism, it appears that in both rats and hamsters estradiol acts to direct metabolic fuels (especially lipids) away from white adipose tissue storage depots and into tissues where they are oxidized (e.g., BAT). Finally, cold acclimation and estradiol had similar effects in OVX hamsters including increases in BAT fatty acid synthesis/uptake, BAT LPL activity, and energy expenditure. These findings, too, are consistent with a role for BAT in estradiol-induced thermogenesis.

Acclimatization↗