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Biomedical subjects

B M Wolfe

Publications and source records attributed to B M Wolfe.

At least 73 records · Page 4Linked to original sources
PubMed1993

Effects of low dosage progestin-only administration upon plasma triglycerides and lipoprotein metabolism in postmenopausal women.

Oral administration to five postmenopausal women of dl-norgestrel (0.075 mg/d for 7 wk) reduced mean fasting plasma levels of triglycerides by 29% (P < 0.001), VLDL triglycerides by 39% (P < 0.01), and VLDL apo B by 26% (P < 0.05), while lowering mean total cholesterol by 7% (P < 0.06). To explain these observations the kinetics of VLDL and LDL apo B turnover were studied by injecting autologous 125I-labeled VLDL and 131I-labeled LDL under control conditions and again in the fourth week of a 7-wk course of dl-norgestrel. VLDL apo B pool size fell by an average of 27% (1.2 vs 1.7 mg/kg, P < 0.06) and production of apo B by 18% (18 vs 22 mg/kg per d, P < 0.05) with unchanged fractional catabolic rate. Production of LDL apo B increased 36% with dl-norgestrel (12 vs 9.4 mg/kg per d, P < 0.05), but this was compensated by a 36% increase in fractional catabolic rate of LDL apo B (0.33 vs 0.25 pools/d, P < 0.005), thereby maintaining pool size. Lipoprotein (a) fell by an average of 12% (16 vs 18 mg/dl, P < 0.06). dl-Norgestrel reduced VLDL triglycerides (40 vs 64 mg/dl, P < 0.05), intermediate density lipoprotein cholesterol (14 vs 19 mg/dl, P < 0.02), IDL apo B (5.3 vs 7.2 mg/dl, P < 0.05), and VLDL cholesterol (3.1 vs 5.1 mg/dl, 0.10 > P > 0.05), in parallel with the reductions in VLDL apo B production and pool size. dl-Norgestrel significantly lowered the production rate of VLDL apo B, thereby decreasing plasma VLDL and intermediate density lipoprotein concentrations.

Aged↗
PubMed1993

The effects of CO2 pneumoperitoneum on hemodynamics in hemorrhaged animals.

BACKGROUND: Carbon dioxide (CO2), the primary gas currently used for pneumoperitoneum, has been known to cause systemic effects on acid-base balance and hemodynamic stability. We studied the hemodynamic effects of CO2 pneumoperitoneum in a hemorrhagic shock model to assess the safety of laparoscopic procedures in acute trauma patients. METHODS: After 1 hour of baseline, 32 anesthetized adult pigs were randomized into four groups. Group 1 animals had no hemorrhage, serving as a control group. Group 2 animals had a mild hemorrhage of 10 ml/kg/hr. Group 3 animals had a moderate hemorrhage of 20 ml/kg/hr. Group 4 animals had a moderate hemorrhage but were resuscitated with 40 ml/kg of lactated Ringer's solution. All animals were then insufflated to an intraabdominal pressure of 15 mm Hg with CO2 gas for 1 hour. The abdomen was then decompressed, and the animals were observed for another hour. All animals survived hemorrhage. One death each occurred in moderate hemorrhage groups, both near the end of CO2 pneumoperitoneum. These animals were not included in statistical analysis. RESULTS: In euvolemic animals, CO2 pneumoperitoneum induced hypercapnia (from 34 +/- 1 mm Hg to 48 +/- 1 mm Hg), acidemia (from 7.45 +/- 0.02 to 7.36 +/- 0.02), and a 20% reduction in stroke volume. Mild hemorrhage and CO2 insufflation resulted in a similar degree of acidemia (7.35 +/- 0.01), but moderate hemorrhage and CO2 insufflation led to more severe acidemia (7.26 +/- 0.02). Fluid resuscitation failed to prevent this severe fall in pH (7.30 +/- 0.03) for group 4. PaCO2 was not affected by hemorrhage, but CO2 pneumoperitoneum induced significant hypercapnia in all groups, ranging from 48 +/- 1 mm Hg for euvolemic animals to 52 +/- 1 mm Hg for moderate hemorrhage animals. Stroke volume declined as a function of blood loss, and it was further depressed by CO2 insufflation, to as low as 75% of baseline in mild hemorrhage and 55% of baseline in moderate hemorrhage. Both stroke volume and cardiac index initially responded to large-volume fluid replacement after moderate hemorrhage but quickly decreased to levels comparable to those of unresuscitated animals when CO2 pneumoperitoneum was created. CONCLUSIONS: Intraperitoneal insufflation with CO2 for diagnostic laparoscopy may be hazardous in acute hypovolemic trauma patients.

Animals↗
PubMed1993

Evidence that cholesteryl ester and triglyceride accumulation in J774 macrophages induced by very low density lipoprotein subfractions occurs by different mechanisms.

The present investigations have examined the mechanism(s) whereby Sf 60-400 very low density lipoproteins (VLDL) from Type IV hypertriglyceridemic subjects cause cholesteryl ester and triglyceride accumulation in J774 macrophages. Both apolipoprotein (apo) E-poor and apoE-rich Type IV VLDL subfractions, isolated by heparin-Sepharose chromatography, were capable of enhancing cellular cholesterol and triglyceride content. The apoE-rich fraction was significantly more effective at inducing cholesterol esterification (P < 0.05) and accumulation of esterified cholesterol (P < 0.05), whereas both subfractions caused similar increases in cellular triglyceride content. Thus, the amount of VLDL-associated apoE determined the extent to which Type IV VLDL loaded J774 cells with cholesterol but not triglyceride. Two VLDL subfractions, Sf 60-400 and Sf 20-60, isolated from Type III subjects homozygous for apoE2, caused little or no effect on cellular esterified cholesterol content, whereas both fractions induced the same degree of cellular triglyceride accumulation as Type IV VLDL. Type IV VLDL-induced cholesteryl ester accumulation was blocked by an anti-apoE monoclonal antibody, known to block the binding of apoE to the LDL receptor; however, the increase in cellular triglyceride was unaffected. Therefore, VLDL-induced triglyceride accumulation in this cell line can occur without apoE-mediated uptake of intact VLDL particles. The addition of heparin to J774 cells resulted in a 6-fold increase in lipoprotein lipase (LPL) activity in the media, and significantly enhanced the ability of Type IV VLDL to induce cellular triglyceride accumulation (P < 0.01), but significantly decreased cellular cholesteryl ester content (P < 0.025). Finally, Sf 60-400 VLDL from two subjects homozygous for apoC-II deficiency failed to increase cellular lipid content. However, the addition of exogenous apoC-II to C-II-deficient VLDL resulted in significant increases of both triglyceride and esterified cholesterol in J774 cells. In the presence of apoC-II, the anti-apoE monoclonal antibody blocked the cellular cholesteryl ester increase induced by C-II-deficient VLDL, but had no effect on the increase in cellular triglyceride. Collectively, these experiments demonstrate that extracellular lipolysis of Sf 60-400 VLDL by LPL is required for cholesteryl ester and triglyceride accumulation in J774 macrophages. After interaction with cellular LPL, VLDL triglycerides are hydrolyzed. The resulting free fatty acids are readily taken up by the macrophage, and re-esterified into triglyceride. Lipolysis proceeds until apoE epitopes are exposed, allowing the triglyceride-depleted remnant, containing all the cholesteryl ester, to be taken up via an apoE-mediated process.

Animals↗
PubMed1992

Lipolysis is a prerequisite for lipid accumulation in HepG2 cells induced by large hypertriglyceridemic very low density lipoproteins.

Lipoprotein kinetic studies have demonstrated that a large proportion of Sf 60-400 very low density lipoprotein (VLDL) is cleared directly from the circulation in Type IV hypertriglyceridemic subjects, at an unknown tissue site. The present studies were designed to investigate the role of hepatocytes in this process and to define the conditions, whereby Type IV Sf 60-400 VLDL would induce lipid accumulation in HepG2 cells. Type IV VLDL (Sf 60-400) failed to augment the total cholesterol, esterified cholesterol, or triglyceride content of HepG2 cells following 24-h incubations. Coincubation of bovine milk lipoprotein lipase (LPL) and Type IV VLDL with HepG2 cells induced a 3-fold increment in cellular esterified cholesterol mass (p less than 0.005) and a 7-fold increase in cellular triglyceride mass (p less than 0.005), compared to VLDL alone. The increased cellular lipid mass was associated with increased oleate incorporation into cellular cholesterol esters and triglycerides. Exogenous LPL hydrolyzed 76% of the VLDL triglyceride over 24 h. LPL action on Type IV VLDL was sufficient to promote cellular uptake of these lipoproteins, while elevated media-free fatty acid levels were not. Although HepG2 cells secrete apolipoprotein (apo) E, we assessed the role of VLDL-associated apoE in the lipid accumulation induced by VLDL plus LPL. ApoE-rich and apoE-poor Type IV VLDL subfractions induced similar increments in cellular esterified cholesterol in the presence of LPL, despite a 4-fold difference in apoE content. Sf 60-400 VLDL, from subjects homozygous for the defective apoE2, plus LPL, behaved identically to Type IV VLDL plus LPL. Type IV VLDL plus LPL, preincubated with anti-apoE (1D7) and apoB (5E11) monoclonal antibodies, known to block the binding of apoE and -B, respectively, to the LDL receptor failed to block lipid accumulation. In contrast, apoE-poor Type IV VLDL, apoE2 VLDL, and VLDL plus 1D7 were taken up poorly by J774 cells, cells that secrete LPL, but not apoE. These studies suggest that lipolytic remodeling of large Type IV VLDL by LPL is a prerequisite for their uptake by HepG2 cells and that HepG2 cell-secreted apoE rather than VLDL-associated apoE is the ligand involved in uptake.

Animals↗
PubMed1992

Intraperitoneal carbon dioxide insufflation and cardiopulmonary functions. Laparoscopic cholecystectomy in pigs.

We studied the effects of laparoscopic cholecystectomy on respiratory and hemodynamic function in eight adult pigs. Minute ventilation was adjusted to normalize baseline arterial blood gases, then fixed throughout carbon dioxide insufflation. A metabolic measurement cart recorded total CO2 excretion, oxygen consumption, and minute ventilation. Carbon dioxide pneumoperitoneum was maintained at a constant pressure of 15 mm Hg as cholecystectomy was performed. After 1 hour of insufflation, CO2 excretion increased from 115 +/- 10 mL/min to 149 +/- 9 mL/min but O2 consumption remained unchanged. The PaCO2 increased from 35 +/- 2 mm Hg to 49 +/- 3 mm Hg and arterial pH fell from 7.47 +/- 0.02 to 7.35 +/- 0.03. Systemic and pulmonary hypertension occurred and stroke volume dropped from 35.5 +/- 3.5 mL to 28.6 +/- 2.2 mL with compensatory tachycardia. Right atrial pressure remained unchanged as inferior vena cava pressure increased to reflect the intraperitoneal pressure. We conclude that CO2 pneumoperitoneum resulted in significant transperitoneal CO2 absorption, with secondary hypercapnia and acidemia. The accumulation of CO2 was also associated with an increase in systemic and pulmonary arterial pressure. Heart rate increased to compensate for the decreased stroke volume to maintain cardiac output.

Acid-Base Equilibrium↗
PubMed1992

Prolonged effects of a novel, low-dosage continuous progestin-cyclic estrogen replacement program in postmenopausal women.

OBJECTIVE: Our objective was to ascertain long-term tolerability and effects of a novel, low-dosage continuous progestin-cyclic estrogen regimen on vasomotor flushing, vaginal bleeding patterns, bone density, and plasma lipoprotein lipids. STUDY DESIGN: Eighteen postmenopausal women with climacteric symptoms received low doses of dl-norgestrel (0.075 mg/day) continuously and 17 beta-estradiol (1 mg/day) intermittently (25 of 28 days) for 3 years. The results were compared with baseline values. RESULTS: The hormonal regimen was well tolerated. Vaginal bleeding, vaginal spotting, and vasomotor flushing occurred in only 0.4%, 4.2%, and 7.7% of cycles, respectively. Bone density was stable. Mean fasting plasma total cholesterol concentration fell 19%, low-density lipoprotein cholesterol 23%, high-density lipoprotein cholesterol 13%, and triglycerides 31% (p less than 0.01) over the 3-year period, while the ratios of low-density lipoprotein cholesterol/high-density lipoprotein cholesterol and total cholesterol/high-density lipoprotein cholesterol decreased by 14% and 10%, respectively. CONCLUSION: Long-term compliance with female hormonal replacement is feasible once vaginal bleeding is essentially eliminated, allowing for potentially better prophylaxis against coronary heart disease, osteoporosis, endometrial cancer, and stroke.

Blood Pressure↗
PubMed1992

Laparoscopic repair of duodenal ulcer and gastroesophageal reflux.

The low morbidity and early recovery associated with laparoscopic procedures have heralded a new era for many types of surgery. In addition to the initial promising reports for duodenal ulcer disease and gastroesophageal reflux discussed above, there is a growing body of reports of gastric procedures performed laparoscopically, including omentopexy for perforated duodenal ulcer and laparoscopic repair of full-thickness stomach injury. Laws et al recently described the use of transthoracic vagotomy in recurrent peptic ulcer disease for four patients who had previously undergone a gastric drainage procedure. As with any new procedure, laparoscopic techniques for duodenal ulcer and Nissen fundoplication reviewed in this section need to be evaluated further for long-term effectiveness and comparability to existing therapy. At least one controlled multicenter trial is ongoing to compare the long-term results and cost-effectiveness of laparoscopic surgery for duodenal ulcer with those of standard medical therapy, and as surgeons gain more experience with these laparoscopic procedures, it is likely that other similar trials will be initiated.

Duodenal Ulcer↗
PubMed1992

Laparoscopic management of the acute abdomen, appendix, and small and large bowel.

The application of laparoscopy for diagnosis and treatment of the acute abdomen, appendicitis, and in the management of small and large bowel diseases is a natural step for the general surgeon. Acute appendicitis is a common general surgical problem that can be difficult to diagnose. Laparoscopy is an excellent aid in diagnosis and laparoscopic appendectomy can be performed easily. The controversy of incidental appendectomy and recommendations for management are discussed. Small and large bowel diseases and their surgical treatment now can be managed laparoscopically thus decreasing morbidity and mortality. The uses and limitations of these techniques are discussed as well as future trends in treatment.

Abdomen, Acute↗
PubMed1992

Effects of gastro-entero-pancreatic hormones upon triglyceride synthesis and secretion by rat hepatocytes.

To ascertain whether certain gastro-entero-pancreatic hormones whose concentration in blood rises after ingestion of food could play a role in the elevation of plasma triglycerides (or hepatic triglyceride secretion) observed after oral vs parenteral feeding, studies were undertaken of their acute effects upon triglyceride synthesis and release by freshly isolated rat hepatocytes in vitro. The incorporation of radiopalmitate into hepatocyte triglycerides was significantly increased, by one-fourth to one-half, by each of pancreatic polypeptide, peptide YY, and an intermediate concentration (0.50 microgram/mL) of somatostatin. However, at a lower concentration (0.25 microgram/mL) somatostatin significantly decreased (by 14%) the incorporation of radiopalmitate into hepatocyte triglycerides. Release of labelled triglycerides from hepatocytes into the medium was significantly enhanced by both gastric inhibitory polypeptide (by 31%) and pancreatic polypeptide (22%), but was significantly reduced (by 28%) by somatostatin at a concentration of 1 microgram/mL. Neurotensin produced no detectable effect. Although there were similarities between the active hormones, each had a unique overall pattern of response on triglyceride synthesis and release and individually, or in concert with other hormones, could modulate hepatic triglyceride production and secretion, thereby explaining the differential effects of oral vs parenteral feeding on plasma triglycerides.

Animals↗
PubMed1992

High protein diet complements resin therapy of familial hypercholesterolemia.

The intermediate-term effects on plasma lipoprotein lipids of substituting meat and dairy protein for carbohydrate in the diets of five subjects (three women, two men) with familial hypercholesterolemia receiving cholestyramine (mean dose, 18 g/d) were studied. Subjects were randomly allocated to either the high or low protein diets (mean 27 versus 10% of energy as protein, 25% as fat, and 48 versus 65% as carbohydrate) for 4 to 5 weeks and then switched to the other diet for another 4 to 5 weeks. Mean fasting plasma HDL cholesterol rose significantly by 17 +/- 3% (1.11 +/- 0.12 vs 0.95 +/- 0.11 mmol/L, p less than 0.005, n = 5), whereas total triglycerides fell by 23 +/- 2% (1.7 +/- 0.3 vs 2.2 +/- 0.3 mmol/L, p less than 0.005, n = 5), VLDL triglycerides fell by 28 +/- 5% (0.88 +/- 0.15 vs 1.18 +/- 0.19 mmol/L, p less than 0.02, n = 5), VLDL cholesterol fell by 32 +/- 7% (0.39 +/- 0.08 vs 0.56 +/- 0.09 mmol/L, p less than 0.01, n = 5), the ratio of LDL cholesterol: HDL cholesterol by 19 +/- 5% (4.7 +/- 0.7 vs 5.7 +/- 0.7, p less than 0.05) and that of total cholesterol: HDL cholesterol by 16 +/- 5% (6.6 +/- 0.5 vs 8.0 +/- 0.7, p less than 0.05) on the high versus low protein diet. Increasing dietary protein intake at the expense of carbohydrate may be useful in treating hypoalphalipoproteinemia and/or hypertriglyceridemia in patients with familial hypercholesterolemia.

Adult↗
PubMed1991

Endoscopic cholecystectomy. An analysis of complications.

We analyzed our initial 381 endoscopic cholecystectomies with particular emphasis on postoperative complications. The rate of conversion to open cholecystectomy was 3%. A technical complication occurred in 2% and a non-technical complication in 4%, for a total complication incidence of 6%. There were three postoperative fatalities (0.9%). Two fatal technical complications consisted of unrecognized intestinal injuries at the time of endoscopic cholecystectomy that were obvious when the abdomen was opened. One patient died of a cerebrovascular accident. Nonfatal technical complications included five bile leaks that required treatment. There were no common bile duct injuries, but excessive caution to prevent common bile duct injury may have contributed to the high incidence of bile leaks. Examination of the case numbers of the technical complications and conversion to open cholecystectomy suggests that the learning curve is real and somewhat prolonged, and that a willingness to convert to open cholecystectomy is necessary if technical complications are to be avoided.

Aged↗
PubMed1991

Changes in cerebrospinal fluid and plasma amino acid concentrations with elevated dietary protein concentration in dogs with portacaval shunts.

Effects of dietary protein concentration on plasma and cerebrospinal fluid (CSF) amino acids (AA) in dogs with portacaval shunts (PCS) were examined. An 18% protein purified diet (18P) was fed to 4 PCS dogs and 2 controls; at week 10, 2 of the PCS dogs were switched to 36% protein (36P) until week 28. Effects of the diet switch on plasma and CSF AA in 8 normal dogs were determined in another experiment. Neither surgery nor protein level significantly affected average food intake (weeks 10-28). Plasma amino acid patterns typical of PCS animals were observed: phenylalanine and tyrosine increased and branched chain AA decreased with shunting (p less than 0.05). Plasma phenylalanine increased further with 36P in PCS dogs (p less than 0.05), but was not affected by dietary protein concentration in controls. With 36P: CSF arginine, serine, histidine, tryptophan, phenylalanine, glutamate and glutamine increased in PCS dogs; but only arginine decreased in CSF of controls (p less than 0.05). In PCS dogs, significant CSF AA changes with elevated dietary protein were unrelated to plasma AA changes.

Amino Acids↗
PubMed1991

Short-term effects of substituting protein for carbohydrate in the diets of moderately hypercholesterolemic human subjects.

The short-term effects on plasma lipoprotein lipids of substituting meat and dairy protein for carbohydrate in the diets of 10 free-living moderately hypercholesterolemic human subjects (four men, six women) were studied under closely supervised dietary control during the consumption of constant, low intakes of fat and cholesterol and the maintenance of stable body weight as well as constant fiber consumption. Subjects were randomly allocated to either the high or low protein diets (mean, 23% v 11% of energy as protein, 24% as fat, and 53% v 65% as carbohydrate) and then switched to the other diet for another 4 to 5 weeks. Mean fasting plasma high-density lipoprotein cholesterol (HDL-C) was significantly higher by 12% +/- 4% (0.97 +/- 0.08 v 0.89 +/- 0.08 mmol/L, P less than .01), whereas mean total cholesterol (TC) was lower by 6.5% +/- 1.3% (5.7 +/- 0.3 v 6.1 +/- 0.3 mmol/L, P less than .001), mean low-density lipoprotein-cholesterol (LDL-C) lower by 6.4% +/- 2.0% (4.5 +/- 0.2 v 4.8 +/- 0.2 mmol/L, P less than .02), mean total triglycerides (TG) lower by 23% +/- 5% (1.7 +/- 0.1 v 2.4 +/- 0.3 mmol/L, P less than .02), and mean high versus low protein diet. Mean values for LDL-C were significantly lower during weeks 3 to 5 of the high protein diet than during either weeks 1 to 5 or weeks 1 to 2 of the high protein diet (4.3 +/- 0.3, 4.5 +/- 0.2, and 4.7 +/- 0.3 mmol/L, respectively, P less than .05) and 11% +/- 3% lower than on low protein diet, P less than .005. The ratio of plasma LDL-C to HDL-C was consistently lower by 17% +/- 3% during the high versus low protein diet (4.9 +/- 0.5 v 5.8 +/- 0.5, P less than .001). Lowering plasma TC and LDL-C and total TG and VLDL-TG and increasing HDL-C by chronic isocaloric substitution of dietary for carbohydrate may enhance the cardiovascular risk reduction obtained by restriction of dietary fat and cholesterol.

Adult↗
PubMed1990

Identification and metabolic characteristics of an apolipoprotein C-II variant isolated from a hypertriglyceridemic subject.

The very low density lipoprotein (VLDL) apolipoproteins from a Type IV hypertriglyceridemic Caucasian subject (plasma TG: 645 mg/dl) and his brother (plasma TG: 328 mg/dl) were separated by isoelectric focusing gel electrophoresis (IEF) and found to contain two isoforms of apoC-II, identified by immunoblot. These corresponded to normal apoC-II-1 (isoelectric point: pI 4.88) and a variant isoform (apoC-II-v, pI 4.74). The pI of C-II-v was not altered by neuraminidase treatment, indicating that it was not sialylated. The concentration of total immunoreactive C-II in VLDL was elevated (18 mg/dl vs normal; 5.0 +/- 2 mg/dl) but similar to that in other Type IV subjects. In VLDL, which contained 90% of the plasma immunoreactive apoC-II, the ratio (by IEF) of C-II-1:C-II-v was 2:1, whereas in high density lipoproteins (HDL) the ratio was 1:1. VLDL apoB turnover was measured after the pulse injection of 125I-labeled VLDL. VLDL apoB kinetic parameters for the proband and four Type IV subjects were similar: production rate, 28 mg/kg per day versus 30 mg/kg per day; fractional catabolic rate, 1.62.day-1 versus 1.96.day-1; and pool size, 17 mg/kg versus 18 mg/kg. The decline in VLDL triglyceride (TG) after the infusion of heparin (9,000 IU over 4 h) was also similar to that observed in Type IV subjects. In VLDL, the fractional catabolic rates of apoC-II-1 and C-II-v were similar (C-II-1: 0.31.day-1, C-II-v: 0.29.day-1) whereas in HDL, although similar to each other, the rates were greater than in VLDL (C-II-1: 0.48.day-1, C-II-v: 0.44.day-1). VLDL and HDL from the proband were normal in their ability to activate bovine skim milk lipase, compared to Type IV VLDL and HDL without C-II-v. Purified apoC-II-1 and apoC-II-v activated the milk lipase to a similar extent (at 1 microgram of C-II; C-II-1: 34 units/h, C-II-v: 35 units/h). Thus, apoC-II-v is a newly recognized isoform of apoC-II-1. It remains to be determined whether this mutation plays a role in the genesis of hypertriglyceridemia.

Adult↗
PubMed1989

Estradiol is a potent inhibitor of the hypotriglyceridemic effect of levonorgestrel in female rats.

The progestin, levonorgestrel, when administered to rats intramuscularly, significantly lowered both total and very low density lipoprotein triglyceride concentrations in the blood plasma by 35-40%. This effect was readily abolished by the simultaneous intramuscular administration of estradiol benzoate. Similarly, estradiol-17 beta overcame the inhibitory effects of levonorgestrel on the incorporation of [9,10-3H]palmitate into triglycerides of freshly isolated rat hepatocytes studied in vitro. However, estradiol alone significantly raised plasma triglycerides by two-fold in vivo. Estradiol also significantly enhanced (by 9%) the incorporation of [9,10-3H]palmitate into hepatocyte triglycerides. These results suggest that the effects of estradiol on triglyceride synthesis and concentration dominate over those of levonorgestrel in the rat.

Animals↗
PubMed1989

Effects of combined estrogen and progestin administration on plasma lipoprotein metabolism in postmenopausal women.

Treatment of postmenopausal women with low doses of estradiol-17 beta (1 mg/d) and dl-norgestrel (0.075 [corrected] mg/d) significantly reduced fasting serum levels of low density lipoprotein (LDL) cholesterol and lowered very low density lipoprotein (VLDL) triglycerides in four of five subjects. To explain these results, the kinetics of VLDL and LDL apolipoprotein (apo) B turnover were studied by injecting autologous 125I-labeled VLDL and 131I-labeled LDL into subjects before discontinuing long-term (4-yr) treatment with the estradiol-17 beta and dl-norgestrel and again 7 wk after stopping treatment. The 24% mean decrease in VLDL apo B pool size during treatment was associated with a significant increase in VLDL apo B fractional catabolic rate (15 +/- 1 vs. 11 +/- 1 pools/d), whereas production rate was similar to control (24 +/- 3 vs. 21 +/- 2 mg/kg per d). There was a significant 25% mean decrease in LDL apo B pool size (27 +/- 2 vs. 36 +/- 3 mg/kg) due to a significant decrease in total (8.3 +/- 0.3 vs. 11 +/- 1 mg/kg per d) and independent (3.3 +/- 0.5 vs. 6.6 +/- 0.8 mg/kg per d, P less than 0.05) LDL apo B production. Estradiol-17 beta together with dl-norgestrel lowered plasma VLDL by enhancing their clearance and LDL by reducing their production.

Apolipoproteins B↗