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Biomedical subjects

H N Ginsberg

Publications and source records attributed to H N Ginsberg.

At least 19 recordsLinked to original sources
PubMed1995

Apoprotein B100, an inefficiently translocated secretory protein, is bound to the cytosolic chaperone, heat shock protein 70.

Apoprotein B100 (apoB) is a secretory protein that appears to be constitutively translated but inefficiently translocated into the lumen of the endoplasmic reticulum. Using several experimental approaches, we found that apoB is bound to the cytosolic chaperone protein, heat shock protein 72/73 (commonly referred to as Hsp70). Similar to other chaperone-protein interactions, this binding was transient and ATP-sensitive. The binding of apoB to Hsp70 in HepG2 cells was decreased by treatment with oleic acid, which increases both translocation and secretion of apoB, and was increased by N-acetyl-leucyl-leucyl-norleucinal, a protease inhibitor which efficiently protects apoB from cellular degradation without affecting translocation. The N-terminal 16% of apoB, which is efficiently translocated into the endoplasmic reticulum lumen in stably transfected Chinese hamster ovary (CHO) cells, showed minimal, if any, binding to Hsp70. The N-terminal 50% of apoB, which is very poorly translocated in CHO cells, was found to bind significantly to Hsp70. These results suggest that domains of nascent apoB localized on the C-terminal regions of the molecule are transiently exposed to the cytosol during translation and/or translocation, and that Hsp70 functions as a molecular chaperone to maintain apoB in a translocational competent conformation until translocation is completed.

Adenosine Triphosphate↗
PubMed1995

Update on the treatment of hypercholesterolemia, with a focus on HMG-CoA reductase inhibitors and combination regimens.

Numerous studies involving patients with hypercholesterolemia have demonstrated that reduction of lipid levels markedly reduces morbidity and mortality from cardiovascular disease. Diet alone may enable patients without established disease to attain target lipid levels, but pharmacotherapy generally is necessary for those with coronary artery disease. Choice of a suitable agent for monotherapy--a bile acid resin, niacin, or an HMG-CoA reductase inhibitor--may be determined by patient phenotype. For resistant cases, therapy combining an HMG-CoA reductase inhibitor with another agent generally is effective and well tolerated.

Cholestyramine Resin↗
PubMed1995

New directions in dietary studies and heart disease: the National Heart, Lung and Blood Institute sponsored Multicenter Study of Diet Effects on Lipoproteins and Thrombogenic Activity.

The National Heart, Blood and Lung Institute-sponsored DELTA study is the first collaborative, multicenter diet study to utilize standardized protocols to feed specific diets to study participants. In the first study, the investigators are focusing on the effects of reducing dietary saturated fat on plasma lipids, lipoproteins, and thrombogenic activity. Future studies will attempt to address important diet/public health questions dealing with high carbohydrate vs. high monounsaturated fat diets, and the cholesterol raising activity of specific saturated fatty acids. Moreover, DELTA will be an invaluable model for other multicenter diet studies.

Adult↗
PubMed1995

Association of postprandial triglyceride and retinyl palmitate responses with newly diagnosed exercise-induced myocardial ischemia in middle-aged men and women.

Although strong evidence exists linking fasting plasma levels of LDL cholesterol (LDL-C) and HDL cholesterol (HDL-C) to risk for development of coronary artery disease (CAD), the data in support of an independent role for fasting triglyceride (TG) concentrations are weak. Humans are in the postprandial state most of the day, however, and results from both basic and clinical studies suggest that postprandial TG levels may be atherogenic. Previous studies have not, however, attempted to determine if postprandial TG levels are associated with CAD independent of other traditional risk factors or plasma lipid levels, particularly fasting plasma concentrations of TG and HDL-C. Ninety-two men and 113 women (mean age, 51.6 and 53.6 years, respectively) were recruited from populations undergoing diagnostic exercise electrocardiographic or thallium stress tests at our medical centers. Twenty-six men and 24 women had positive tests. We chose exercise-induced myocardial ischemia (EIM) as the criterion for defining case and control subjects because we wanted participants who did not have a prior diagnosis of CAD. Blood samples were obtained for measurement of plasma TG, TG-rich lipoprotein TG, and retinyl palmitate (RP) levels 2, 3.5, 5, and 8 hours after the subjects had consumed a fatty test meal. Logistic regression models were developed to test for associations between each variable and case-control status. Among men but not women postprandial TG and RP responses were associated with EIMI independent of age, race, and smoking status. In the male group, the odds ratio (OR) for an increase in postprandial TG response of approximately 1 SD was 1.69 (P = .007); the OR for an increase in RP response of 1 SD was 2.47 (P = .011). However, when fasting TG was added to the model, the OR for postprandial TG area in the men was reduced to 1.44 (P = .17); the OR postprandial RP area in the men was reduced to 1.88 (P = .12). There was no effect of adding other risk factors, including LDL-C and HDL-C, to the model. Significant effect modification by body mass index (BMI) on the relationship between postprandial responses and case-control status was observed. In men with BMI < 30, the OR was 1.83 for postprandial TG (P = .041) and 2.77 for postprandial RP (P = .032) in models that included fasting TG, LDL-C, and hypertension.

Age Factors↗
PubMed1995

Increases in dietary cholesterol are associated with modest increases in both LDL and HDL cholesterol in healthy young women.

We studied the effects of dietary cholesterol intake on lipid and lipoprotein levels in healthy young women (n = 13) who were otherwise eating an American Heart Association (AHA) diet. The study used a randomized, three-way crossover design to determine the effects of 0, 1, or 3 eggs added per day (dietary cholesterol range, 108 to 667 mg/d). Each of the three diets was eaten for 8 weeks, with a washout period between diets. Three fasting blood samples were obtained during the last 3 weeks of each diet period to observe changes in fasting plasma lipid levels associated with the menstrual cycle. We also obtained blood just before and 4 and 8 hours after the subjects ingested a standard high-fat formula. During the menstrual cycle, total cholesterol and LDL cholesterol levels fell by 0.051 mmol/L (1.99 mg/dL) and 0.064 mmol/L (2.48 mg/dL) per week, respectively. HDL cholesterol concentrations increased by 0.060 mmol/L (2.3 mg/dL) per week during the first half of the cycle and then fell by 0.050 mmol/L (1.94 mg/dL) per week during the second half. Therefore, all statistical analyses were performed on values adjusted to midcycle. Total fasting cholesterol concentrations increased by 0.073 mmol/L (2.81 mg/dL) per 100 mg dietary cholesterol added to the diet per day (P = .001). LDL cholesterol increased by 0.054 mmol/L (2.08 mg/dL) per 100 mg/d dietary cholesterol (P = .003); this accounted for about 75% of the rise in total cholesterol. HDL cholesterol concentrations increased by 0.015 mmol/L (0.57 mg/dL) per 100 mg/d dietary cholesterol (P < .04). There was a wide range of responses among the women. Plasma apoB levels increased significantly, 0.93 mg/dL per 100 mg/d dietary cholesterol (P = .025), whereas apoA-I levels tended to rise (1.35 mg/dL per 100 mg/d, P = .056). Increases in dietary cholesterol did not produce any observable effects on fasting plasma cholesteryl ester transfer protein levels and had no effect on the response to a standard high-fat formula. Although menstrual-cycle changes in plasma total, LDL, and HDL cholesterol levels were observed, the effects of the diets were similar in the follicular and luteal phases of the menstrual cycle. Additionally, despite changes associated with the menstrual cycle, within-subject variation in plasma total cholesterol was actually smaller in this study than in our study of young men.

Adult↗
PubMed1992

Studies of the sites of intracellular degradation of apolipoprotein B in Hep G2 cells.

We previously reported that treatment of Hep G2 cells with oleate significantly increased apolipoprotein B (apoB) secretion by reducing early intracellular degradation of nascent apoB. In the current study, inhibitors of secretory protein transport (brefeldin A and monensin), cell fractionation studies, and protease protection assays were utilized to determine the location of apoB degradation and to better define the mechanism whereby oleate treatment reduces nascent apoB intracellular degradation. When cells were treated with brefeldin A, which blocks endoplasmic reticulum (ER) to Golgi protein transport, apoB degradation continued in control cells, suggesting that apoB is degraded in the ER. When oleate-treated cells were blocked with brefeldin A, oleate failed to protect apoB from intracellular degradation. The effects of brefeldin A were not due to effects on lipid synthesis as brefeldin A did not inhibit the synthesis of triglyceride, phospholipid, free cholesterol, or cholesteryl ester in control cells and did not prevent the increases in triglyceride (14-fold) and phospholipid (1.4-fold) synthesis seen in oleate-treated cells. Simultaneous treatment of cells with brefeldin A and nocodazole, which inhibits retrograde transport of proteins from Golgi to ER, added to the evidence for the ER as the site of apoB degradation. This conclusion received further support from experiments in which cells were treated with monensin, a Na+ ionophore which halts protein secretion at the level of the trans-Golgi network. Early degradation of nascent apoB (between 10 and 20 min of chase) was observed in monensin-treated cells, but then cellular apoB degradation ceased and apoB was stable during the remaining chase period. More apoB accumulated in the Golgi of cells that had been treated with oleate and monensin. These results suggest that ER degradation occurs in monensin-treated cells, but then stops as apoB is transferred to the Golgi. The results obtained in whole cells were confirmed in studies using isolated ER and Golgi, which indicated that ER contains a proteolytic activity which degrades apoB, in vitro, whereas Golgi does not. ApoB degradation in isolated ER was not reduced by pretreatment with oleate. Finally, protease protection assays carried out with isolated microsomes indicated that a majority of the apoB in both control or oleate-treated HepG2 cells was located on the cytosolic side of the membranes.(ABSTRACT TRUNCATED AT 400 WORDS)

Albumins↗
PubMed1992

Effects of lovastatin therapy on very-low-density lipoprotein triglyceride metabolism in subjects with combined hyperlipidemia: evidence for reduced assembly and secretion of triglyceride-rich lipoproteins.

We have previously reported decreased production rates of the major apolipoprotein B (apoB)-containing lipoproteins, very-low-density lipoproteins (VLDL), and low-density lipoproteins (LDL) in patients with combined hyperlipidemia (CHL) during treatment with lovastatin. In the present study, we determined the effects of lovastatin therapy on VLDL triglyceride (TG) metabolism. Plasma VLDL turnover was determined in six CHL patients, before and during lovastatin therapy. 3H-triglyceride-glycerol-specific activity data derived from injection of 3H-glycerol were analyzed by compartmental modeling. The effects of lovastatin on VLDL TG metabolism were compared with those previously determined on VLDL apoB metabolism in these subjects. Lovastatin therapy was associated with decreased concentrations of VLDL TG in five of six patients and decreased VLDL apoB concentrations in all six. VLDL TG production rates (PR) decreased in five patients, with the mean for the group decreasing from 14.1 +/- 7.1 to 10.3 +/- 4.0 mg/kg/h (P less than .05). VLDL apoB PR also decreased in five patients, with the mean decreasing from 21.8 +/- 20.3 to 12.2 +/- 9.0 mg/kg/d (P = .11). Changes in VLDL TG concentrations during lovastatin treatment were correlated with changes in VLDL apoB concentrations (r = .74, P = .09) and in VLDL TG PR (r = .91, P = .01). Changes in VLDL TG PR were also related to changes in VLDL apoB PR (r = .62, P = NS). There were no consistent changes in the fractional catabolic rates of either VLDL TG or VLDL apoB during lovastatin therapy.(ABSTRACT TRUNCATED AT 250 WORDS)

Apolipoproteins B↗
PubMed1992

Hepatic synthesis of lipoproteins and apolipoproteins.

We have attempted to review new information concerning the regulation of the secretion of three major apolipoproteins that are synthesized in the liver: apoB, apoA-I, and apoE. ApoB, which is a large protein involved in the transport of triglyceride and cholesterol from the liver to the peripheral tissues, appears not to be regulated on a short-term basis at the transcriptional level. Rather, once synthesized, this protein, which is unique in its intracellular transport in the secretory pathway, is subjected to post-translational regulation, which is dependent on the lipid status of the cell. Assembly of nascent apoB-containing LPs begins in the ER. If core lipids, whether triglyceride or cholesteryl ester, are limiting, then apoB will be rapidly degraded, most likely in the ER compartment. However, if one or both of the core lipids are available in adequate quantities, then apoB will be protected in the ER, and more apoB, in the form of an apoB-containing LP (whether VLDL or a smaller particle) will be secreted by the hepatocyte. Addition of surface lipids, mainly phospholipids or free cholesterol, probably occurs in the Golgi. A further mechanism that regulates the secretion of apoB-containing LPs may involve rapid reuptake of newly secreted particles. The regulation of the secretion of apoA-I by liver is very different from that of apoB. Although apoA-I is also synthesized on attached ribosomes and becomes contranslationally or post-translationally associated with the RER membrane, it is transported to the Golgi much more rapidly than apoB. In the Golgi nascent HDL particles are formed, but it is also likely that apoA-I is secreted by the hepatocyte in a lipid-poor form.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Reducing total dietary fat without reducing saturated fatty acids does not significantly lower total plasma cholesterol concentrations in normal males.

Forty-eight healthy male students ate an average American diet (AAD) with 37% of calories from fat and 16% from saturated fatty acids for 3 wk. During the next 7 wk, one-third of the students continued to eat the AAD, one-third switched to a 30%-fat diet with 9% saturated fatty acids (Step 1 diet), and one-third switched to a 30%-fat diet with 14% saturated fatty acids (Sat diet). The Step 1 group had a significant reduction in plasma total cholesterol (TC) (0.36 +/- 0.37 mmol/L) compared with the AAD group (0.07 +/- 0.39 mmol/L) and the Sat group (0.08 +/- 0.25 mmol/L). The Sat group did not differ from the AAD group. Changes in low-density-lipoprotein (LDL) cholesterol paralleled changes in total cholesterol. High-density-lipoprotein cholesterol fell significantly in the Step 1 group (0.11 +/- 0.08 mmol/L) compared with the AAD group. Plasma triglycerides did not differ between groups at the end of the randomized periods. In summary, reduction of dietary fat intake from 37% to 30% of calories did not lower plasma total and LDL cholesterol concentrations unless the reduction in total fat was achieved by decreasing saturated fatty acids.

Adult↗
PubMed1992

Mechanism of hypertriglyceridemia in human apolipoprotein (apo) CIII transgenic mice. Diminished very low density lipoprotein fractional catabolic rate associated with increased apo CIII and reduced apo E on the particles.

Hypertriglyceridemia is common in the general population, but its mechanism is largely unknown. In previous work human apo CIII transgenic (HuCIIITg) mice were found to have elevated triglyceride levels. In this report, the mechanism for the hypertriglyceridemia was studied. Two different HuCIIITg mouse lines were used: a low expressor line with serum triglycerides of approximately 280 mg/dl, and a high expressor line with serum triglycerides of approximately 1,000 mg/dl. Elevated triglycerides were mainly in VLDL. VLDL particles were 1.5 times more triglyceride-rich in high expressor mice than in controls. The total amount of apo CIII (human and mouse) per VLDL particle was 2 and 2.5 times the normal amount in low and high expressors, respectively. Mouse apo E was decreased by 35 and 77% in low and high expressor mice, respectively. Under electron microscopy, VLDL particles from low and high expressor mice were found to have a larger mean diameter, 55.2 +/- 16.6 and 58.2 +/- 17.8 nm, respectively, compared with 51.0 +/- 13.4 nm from control mice. In in vivo studies, radiolabeled VLDL fractional catabolic rate (FCR) was reduced in low and high expressor mice to 2.58 and 0.77 pools/h, respectively, compared with 7.67 pools/h in controls, with no significant differences in the VLDL production rates. In an attempt to explain the reduced VLDL FCR in transgenic mice, tissue lipoprotein lipase (LPL) activity was determined in control and high expressor mice and no differences were observed. Also, VLDLs obtained from control and high expressor mice were found to be equally good substrates for purified LPL. Thus excess apo CIII in HuCIIITg mice does not cause reduced VLDL FCR by suppressing the amount of extractable LPL in tissues or making HuCIIITg VLDL a bad substrate for LPL. Tissue uptake of VLDL was studied in hepatoma cell cultures, and VLDL from transgenic mice was found to be taken up much more slowly than control VLDL (P < 0.0001), indicating that HuCIIITg VLDL is not well recognized by lipoprotein receptors. Additional in vivo studies with Triton-treated mice showed increased VLDL triglyceride, but not apo B, production in the HuCIIITg mice compared with controls. Tissue culture studies with primary hepatocytes showed a modest increase in triglyceride, but not apo B or total protein, secretion in high expressor mice compared with controls. In summary, hypertriglyceridemia in HuCIIITg mice appears to result primarily from decreased tissue uptake of triglyceride-rich particles from the circulation, which is most likely due to increased apo CIII and decreased apo E on VLDL particles. the HuCIIITg mouse appears to be a suitable animal model of primary familial hypertriglyceridemia, and these studies suggest a possible mechanism for this common lipoprotein disorder.

Animals↗
PubMed1992

Increased concentration of plasma cholesteryl ester transfer protein in nephrotic syndrome: role in dyslipidemia.

Hyperlipidemia is a prominent feature of the nephrotic syndrome. Lipoprotein abnormalities include increased very low and low density lipoprotein (VLDL and LDL) cholesterol and variable reductions in high density lipoprotein (HDL) cholesterol. We hypothesized that plasma cholesteryl ester transfer protein (CETP), which influences the distribution of cholesteryl esters among the lipoproteins, might contribute to lipoprotein abnormalities in nephrotic syndrome. Plasma CETP, apolipoprotein and lipoprotein concentrations were measured in 14 consecutive untreated and 7 treated nephrotic patients, 5 patients with primary hypertriglyceridemia, and 18 normolipidemic controls. Patients with nephrotic syndrome displayed increased plasma concentrations of apoB, VLDL, and LDL cholesterol. The VLDL was enriched with cholesteryl ester (CE), shown by a CE/triglyceride (TG) ratio approximately twice that in normolipidemic or hypertriglyceridemic controls (P < 0.001). Plasma CETP concentration was increased in patients with untreated nephrotic syndrome compared to controls (3.6 vs. 2.3 mg/l, P < 0.001), and was positively correlated with the CE concentration in VLDL (r = 0.69, P = 0.004) and with plasma apoB concentration (r = 0.68, P = 0.007). Treatment with corticosteroids resulted in normalization of plasma CETP and of the CE/TG ratio in VLDL. An inverse correlation between plasma CETP and HDL cholesterol was observed in hypertriglyceridemic nephrotic syndrome patients (r = -0.67, P = 0.03). The dyslipidemia of nephrotic syndrome includes increased levels of apoB-lipoproteins and VLDL that are unusually enriched in CE and likely to be atherogenic. Increased plasma CETP probably plays a significant role in the enrichment of VLDL with CE, and may also contribute to increased concentrations of apoB-lipoproteins and decreased HDL cholesterol in some patients.

Adult↗
PubMed1991

Oleate stimulates secretion of apolipoprotein B-containing lipoproteins from Hep G2 cells by inhibiting early intracellular degradation of apolipoprotein B.

Studies were conducted to explore the effects of oleate addition on the secretion of apolipoprotein B (apoB)-containing lipoproteins from Hep G2 cells. Whether oleate was added simultaneously with [3H]-leucine or added to prelabeled cells, the rate of secretion of apoB was stimulated more than 100% within 40 min. When oleate was withdrawn from the cells, the rate of secretion returned to the prestimulated rate within 40 min. These observations suggested that oleate affects apoB secretion early in the secretory pathway. When the effects of oleate on apoB secretion were studied in pulse-chase experiments, it was observed that although apoB synthesis was not affected, apoB intracellular degradation was significant inhibited by oleate. In the absence of oleate, 58% of apoB synthesized during the labeling period was degraded within 20 min, before secretion of apoB into the media had begun, whereas only 29% of labeled apoB was degraded intracellularly during this same time period when oleate was present. Thus, it appears that oleate rapidly stimulates the secretion of apoB by protecting nascent apoB from degradation early in the secretory pathway. Furthermore, stimulation of apoB secretion was observed over a range that includes physiological concentrations of oleate, from 0.1 mM (oleate: bovine serum albumin ratio = 0.45) to 0.8 mM (oleate: ratio = 3.6), suggesting that exogenous oleate could be a physiological modulator of apoB secretion.

Albumins↗
PubMed1991

Lipoprotein physiology in nondiabetic and diabetic states. Relationship to atherogenesis.

Abnormalities of plasma lipid and lipoprotein concentrations are common in both insulin-dependent (IDDM) and non-insulin-dependent (NIDDM) diabetes mellitus. In general, individuals with IDDM who are untreated or inadequately treated have elevations in both postprandial and fasting triglyceride levels in association with reduced activity of lipoprotein lipase. Low-density lipoprotein (LDL) cholesterol levels can rise when insulin deficiency impacts on LDL-receptor function. When patients with IDDM are treated and plasma glucose levels well controlled, plasma very-low-density lipoprotein (VLDL) triglyceride and LDL cholesterol levels are usually normal. In addition, plasma high-density lipoprotein (HDL) cholesterol levels are normal or elevated in well-controlled IDDM subjects. In NIDDM, increased VLDL triglyceride and reduced HDL cholesterol concentrations are common and are only partially related to glycemic control. Overproduction of VLDL leads to hypertriglyceridemia, which can be exacerbated if lipoprotein lipase activity is also reduced. The regulation of LDL levels is complex; catabolism can be reduced if significant insulin deficiency exists or increased if significant hypertriglyceridemia is present. The reduced levels of HDL cholesterol in NIDDM appear to be related to increased exchange of HDL cholesteryl esters for VLDL triglycerides, although other mechanisms may exist. The roles of insulin resistance, obesity, and independently inherited abnormalities of lipoprotein metabolism in the etiology of dyslipidemia of NIDDM are complex and require further investigation. Finally, the effects of diabetes on glycosylation of apoproteins; on other lipid enzymes, particularly hepatic triglyceride lipase; on lipoprotein surface lipids; and on hepatic uptake of remnants have only just begun to be defined. In view of the marked increase in atherosclerotic cardiovascular disease in individuals with diabetes mellitus, prompt attention to and aggressive therapy for dyslipidemia should be a central component of care for these patients.

Apolipoproteins↗
PubMed1990

Reduction of plasma cholesterol levels in normal men on an American Heart Association Step 1 diet or a Step 1 diet with added monounsaturated fat.

The design of diets to achieve optimal changes in plasma lipid levels is controversial. In a randomized, double-blind trial involving 36 healthy young men, we evaluated the effects on plasma lipid levels of both an American Heart Association Step 1 diet (in which 30 percent of the total calories were consumed as fat: 10 percent saturated, 10 percent monounsaturated, and 10 percent polyunsaturated fats, with 250 mg of cholesterol per day) and a monounsaturated fat-enriched Step 1 diet (with 38 percent of the calories consumed as fat: 10 percent saturated, 18 percent monounsaturated, and 10 percent polyunsaturated fats, with 250 mg of cholesterol per day). The effects of these diets were then compared with those of an average American diet, in which 38 percent of the total calories were consumed as fat: 18 percent saturated, 10 percent monounsaturated, and 10 percent polyunsaturated fats, with 500 mg of cholesterol per day. The men consumed the average American diet for 10 weeks before random assignment to one of the two Step 1 diets or to continuation of the average diet for an additional 10 weeks. Caloric intake was adjusted to maintain a constant body weight. As compared with the mean (+/- SD) change in the plasma total cholesterol level in the group that followed the average American diet throughout the study (-0.05 +/- 0.36 mmol per liter), there were statistically significant reductions (P less than 0.025) in the plasma total cholesterol level in the group on the Step 1 diet (-0.37 +/- 0.27 mmol per liter) and in the group on the monounsaturated fat-enriched Step 1 diet (-0.46 +/- 0.36 mmol per liter). There were parallel reductions in the plasma low-density lipoprotein cholesterol levels in these two groups. Neither the plasma triglyceride levels nor the high-density lipoprotein cholesterol concentrations changed significantly with any diet. We conclude that enrichment of the Step 1 diet with monounsaturated fat does not alter the beneficial effects of the Step 1 diet on plasma lipid concentrations.

Adult↗
PubMed1990

Lack of effect of dehydroepiandrosterone in obese men.

To assess the effects of dehydroepiandrosterone (DHEA) on weight and body fat mass in young obese men, six obese (body mass index, 31.5 +/- 2.9 (s.e.] men were studied at baseline, after 28 days of placebo administration, and again after 28 days of DHEA (1600 mg/day) administration. Body fat mass was assessed on each occasion by three separate methods: hydrostatic weighing, impedance plethysmography, and skinfold measurements at four body sites. Waist-to-hip ratios were recorded. In addition, tissue sensitivity to insulin was determined using the modified minimal model technique, and serum lipids were assayed. Serum DHEA-sulfate levels rose from 7.4 +/- 1.7 mumol/l at baseline to 39.8 +/- 11.9 mumol/l after DHEA administration (P less than 0.05). Although body fat mass was reduced in two of the six men following DHEA administration, for the group as a whole neither total body weight, body fat mass, or waist-to-hip ratio changed significantly during the study. No change in either tissue insulin sensitivity or serum lipids was observed. These observations suggest that, at a daily dose of 13.4-19.7 mg/kg, short-term DHEA administration does not affect the total weight, body fat mass, fat distribution, insulin sensitivity, or lipid status of obese young men.

Adipose Tissue↗