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PubMed1985

Augmentation of unesterified arachidonic acid in the renal inner medulla of dexamethasone-treated rats. Relationship to altered triglyceride metabolism.

The present study was designed to investigate the effect of dexamethasone treatment for 2 weeks (2.5 mg/kg/week, subcutaneously) on the level of unesterified fatty acids, particularly arachidonic acid, in the renal medulla of rats, and to relate the observed effect to changes in the tissue concentration and the fatty acid composition of renal medulla phospholipids and triglycerides. Dexamethasone treatment caused an increase in the renal inner medulla level of unesterified fatty acids, including arachidonic acid, that was associated with a reduction of triglycerides and of arachidonic acid esterified into triglycerides, and with an increase in the rate of fatty acids esterification into triglycerides. In contrast, dexamethasone treatment did not affect the renal medulla concentration of phospholipids, the arachidonic acid content of renal medulla phospholipids, or the rate of esterification of fatty acids into renal medulla phospholipids. In the face of increased fatty acid esterification into triglycerides, the finding of reduced triglyceride levels in the renal medulla of dexamethasone-treated rats suggests excessive triglyceride breakdown. If so, fatty acids including arachidonic acid liberated from triglycerides may contribute to elevation of unesterified fatty acid levels in the renal medulla during dexamethasone treatment. The increased level of free arachidonic acid in the renal medulla of dexamethasone-treated rats may explain in part the reported effect of this steroid in increasing urinary prostaglandins.

Animals↗
PubMed1979

Norethindrone acetate inhibition of splanchnic triglyceride secretion in conscious glucose-fed siwne.

The effects of conventional doses of two synthetic contraceptive steroids on the concentration and rate of secretion of plasma triglycerides from the splanchnic region were investigated. Studies were undertaken in miniature swine under steady state conditions produced by prolonged constant hypercaloric intravenous infusions of glucose. The steroids, alone or in combination, were administered with the high carbohydrate diet for at least 2 weeks prior to study of splanchnic metabolism and were also infused intravenously during the studies. Splanchnic triglyceride secretion was determined from measurements of plasma flow and transsplanchnic radiochemical gradients of plasma triglycerides. Compared with studies in the untreated animal, norethindrone acetate significantly reduced the arterial concentration (1.1 +/- 0.1 vs. 0.7 +/- 0.1 mM) and rate of splanchnic secretion of plasma triglyceride fatty acids (2.0 +/- 0.4 vs. 0.8 +/- 0.1 micro mol/min.kg body wt(0.75)) and decreased the percent of free fatty acids entering the splanchnic region that was converted to plasma triglycerides (22 +/- 5 vs. 13 +/- 3%, P < 0.05). Ethynylestradiol, in the dose employed, had no significant effect on these variables; however, ethynylestradiol and norethindrone acetate together gave responses similar to norethindrone acetate alone. When the glucose was given intraduodenally vs. intravenously, values for splanchnic metabolism of triglycerides were unchanged. The hypolipemic effect of norethindrone acetate in glucose-fed swine was attributable to inhibition of hepatic triglyceride secretion.-Wolfe, B. M., and D. M. Grace. Norethindrone acetate inhibition of splanchnic triglyceride secretion in conscious glucose-fed swine.

Animals↗
PubMed1972

Uptake and metabolism of circulating chylomicron triglyceride by rabbit aorta.

To determine if chylomicron triglycerides are taken up and metabolized by the arterial wall, rabbit abdominal aortas were perfused in situ for various times up to 2 hr with blood-buffer containing isotopically labeled substrates. Labeled chylomicrons were obtained by feeding [(3)H]palmitic acid or [(3)H]glyceryl trioleate to rats and rabbits with cannulated thoracic ducts. After aortic perfusion with these chylomicrons, more than 85% of aortic lipid ester radioactivity was in triglyceride; when labeled glycerol or palmitic acid was perfused, most aortic ester lipid radioactivity was in diglycerides and phospholipids. This indicated that, during perfusion with chylomicrons, intact triglyceride molecules were taken up by aorta. The rate of triglyceride fatty acid uptake by the inner avascular segment approached maximal values at low concentrations of perfusate triglyceride fatty acids (2 mm), whereas uptake in the outer capillary perfused segment increased with increasing triglyceride fatty acid concentration (0.4-25 mm). By double-radioisotope techniques it was shown that aortic free fatty acid was derived from both perfusate free fatty acids and from hydrolysis of lipoprotein glycerides within the aortic wall. Uptake of chylomicron triglyceride by perfused aorta was independent of triglyceride hydrolysis, which was quantitatively small.

Animals↗
PubMed1978

[Human catabolism of medium and long chain triglycerides after intravenous infusion].

The metabolic rate of intravenously administered middle-chain and long-chain triglycerides has been tested in metabolically healthy adult subjects. After an infusion period of three hours (infusion rate 0.22 g triglyceride/kg body-weight and hour) the metabolic rate of long-chain triglycerides was 16.4 mg/kg body-weight and hour. The metabolic rate of the middle-chain triglycerides (infusion rate 0.056 g/kg body-weight and hour) administered in a mixture with long-chain triglycerides was slower: 4.8 mg/kg body-weight and hour. Even under these conditions, middle-chain triglycerides increased ketonemia and ketonuria. Furthermore, the acetate level in blood increased significantly. Infusion of lipids have a strong effect on amino-acid levels in blood. The concentration of alanine, leucine, isoleucine are decreased, whereas the concentration of glutamate increases at the same time. Under clinical parameters only a mild leucocytosis has been found. Our data suggest that the metabolic rate of middle-chain triglycerides is according to their low plasma concentration slow, nevertheless, the ketogenesis is significantly higher if middle-chain triglycerides are infused in a mixture with long-chain triglycerides.

Acetates↗
PubMed1968

Choline-deficiency fatty liver: impaired release of hepatic triglycerides.

After intravenous injection of palmitate-1-(14)C to rats fed a choline-deficient (CD) or choline-supplemented (CS) diet for 15-18 hr, liver triglycerides became labeled very rapidly. In CS, but not in CD rats, there was a considerable loss, with time, of radioactivity from liver triglycerides. At the same time, significantly less radioactivity appeared in plasma triglycerides of CD rats than of CS animals. No difference was seen in the triglyceride content of microsomes isolated from the liver of rats fed the two diets. The lower radioactivity in plasma triglycerides of CD rats was essentially due to a lower level and specific activity of very low density lipoprotein triglycerides. After intravenous injection of Triton and labeled palmitate, considerably less radioactivity accumulated in plasma triglycerides and phospholipids of CD rats than of CS animals. Post-Triton hyperphospholipidemia was also less pronounced in CD rats. It was concluded that the fatty liver observed in CD rats results from an impaired release of hepatic triglycerides into plasma.

Animals↗
PubMed1982

Serum triglyceride levels in newborns and mothers at parturition.

From August 1980 to March 1981, paired cord venous blood and maternal antecubital venous blood were measured for triglyceride concentrations with the enzymatic method of triglyceride G-3-PDH UV end point assay, using the Hitachi Model 716 autoanalyser. The mean value of cord serum triglyceride concentrations in the cohort of 100 normal newborns was 28 ng/100 ml and the cut-off point of P95 was 48 mg/100 ml. In normotriglyceridemic newborns and hypertriglyceridemic newborns the mean values were 29 mg/100 ml and 66 mg/100 ml, respectively. However, the mean values of the corresponding triglyceride concentrations of maternal blood were not remarkably different among these 3 groups; they ranged from 190 to 193 mg/100 ml. The cord blood triglyceride level was much lower than that of maternal blood levels, with a ratio of 15% in the cohort of normal population of newborns and mothers. These findings showed that the cord serum triglyceride level was independent of the maternal serum triglyceride concentration and was of fetal origin. The relative impermeability of the placenta to this serum constituent and the lack of utilization of fat as a major source of energy in the period of normal intrauterine fetal life may, in part, account for the low serum triglyceride level in cord blood.

Female↗
PubMed1994

Gestational age dependency of essential fatty acids in cord plasma cholesterol esters and triglycerides.

Plasma cholesterol ester and triglyceride fatty acid compositions of 38 singleton deliveries (23-42 wk), three twins (32, 39, and 40 wk), and their mothers were investigated. No gestational age-dependent changes occurred in maternal fatty acid compositions. Long-chain polyunsaturated fatty acids in fetal cholesterol esters and triglycerides were higher, and their precursors (18:2c,omega 6 and 18:3c,omega 3) were lower than those in corresponding maternal lipid classes. Except for 22:6c,omega 3,20:2c,omega 6, and 22:5c,omega 6, all long-chain polyunsaturated fatty acids in fetal triglycerides increased with advancing gestation. Fetal triglyceride 22:6c,omega 3/22:5c,omega 3 ratio decreased, whereas 22:5c,omega 6/22:4c,omega 6 remained constant. Fetal cholesterol ester and triglyceride 20:3c,omega 9 contents were higher than those of corresponding maternal fractions and did not change with gestation. Triglyceride 18:2c,omega 6 contents of babies with gestational ages of more than 34 wk were linearly related to those of their mothers. The data suggest that increasing triglyceride long-chain polyunsaturated fatty acid content with advancing gestation is partially caused by delta 6- and delta 5-desaturase maturation in the liver. Constancy of 22:6c,omega 3 and 22:5c,omega 6/22:4c,omega 6 and decrease of 22:6c,omega 3/22:5c,omega 3 in triglycerides may point to low hepatic delta 4-desaturation. Transplacental transport of 20:3c,omega 9, following by fetal conservation, should be considered. High 18:2c,omega 6 and low 18:3,omega 3 intakes by the mother may unfavorably influence fetal production of 22:6c,omega 3 in the liver. Because of low hepatic delta 4-desaturation capacity the influence may be small, however.

Cholesterol↗
PubMed1996

[Reproducibility of fasting serum cholesterol and triglycerides in ambulatory patients with mixed hyperlipidemia].

Intraindividual variability of serum lipid concentrations in normal volunteers and in patients with hyperlipidemia is substantial. The aim of this study was to investigate prospectively the reproducibility of fasting serum triglyceride and total cholesterol concentrations in primary health care patients with combined hyperlipidemia, i.e. under conditions of daily medical practice. Secondary forms of hyperlipidemia were excluded. 19 general medical outpatients with primary combined hyperlipidemia were studied. Serum total cholesterol and triglyceride concentrations were measured after an overnight fast at 08.00 h 4 times at weekly intervals. To study the influence of alcohol intake on serum lipid concentrations, total cholesterol and triglycerides were measured without alcohol influence and 12 hours after consumption of a mean of 100 g alcohol in the evening. In 19 patients (10 males, 9 females, mean age 55 years, body mass index 27.9 +/- 4.4 kg/m2), mean +/- SD of serum triglycerides was 3.97 +/- 1.8 mmol/l and of total cholesterol 7.9 +/- 1.8 mmol/l. The combined intraindividual and interassay coefficient of variation was 18.7 +/- 8.2% for triglycerides and 5.1 +/- 2.5% for total cholesterol. Fasting serum triglycerides (3.5 +/- 1.1 vs. 3.7 +/- 1.4 mmol/l) and total cholesterol (7.6 +/- 1.4 vs. 7.8 +/- 1.0 mmol/l) did not significantly change 12 hours after acute alcohol consumption. Patients with primary combined hyperlipidemia in a primary health care setting show small intraindividual variations of overnight fasted serum triglyceride and total cholesterol concentrations. Moderate alcohol consumption 12 hours before blood sampling does not significantly affect triglyceride and cholesterol values.

Adult↗
PubMed1997

The impact of physiological insulin concentration and depletion on the metabolism of glucose, endogenous glycogen, and triglycerides in the isolated perfused heart.

In isolated nonworking hearts perfused with substrate-free medium for 90 min, 2000 microU insulin.mL-1 reduced the rates of glycogenolysis and lipolysis, whereas 50 microU insulin.mL-1 reduced the rate of lipolysis with no significant effect on glycogenolysis. Glycogen and triglycerides were the chief energy sources during the course of depletion in the presence and absence of insulin. In hearts perfused with medium containing 5 mM glucose for 3 h, glycogen and triglycerides contributed to the heart energy requirement, but in the presence of insulin (50 or 2000 microU.mL-1) endogenous triglycerides contributed to the heart energy requirement with net glycogen synthesis. In hearts preperfused with substrate-free medium for 90 min and perfused for another 90 min with medium containing 5 mM glucose, the depletion of endogenous glycogen and triglycerides stimulated the utilization of glucose and the synthesis of glycogen and triglycerides. In hearts preperfused with substrate-free medium for 90 min and perfused for another 90 min with medium containing glucose (5 mM) and insulin (50 or 2000 microU.mL-1), insulin enhanced the utilization of glucose and the synthesis of glycogen and triglycerides. Glucose utilization, glycogenolysis, lipolysis, and synthesis of glycogen and triglycerides were sensitive to the physiological insulin concentration and were also affected by the heart content of glycogen and triglycerides, in the isolated nonworking perfused rat heart.

Animals↗
PubMed1976

[Digestion and absorption of dietary triglycerides].

This review is an attempt to put in order some facts obtained during twenty-five years of studying the digestion and absorption of dietary triglycerides. After a short history of this problem to show the progress of research, the active mechanism of pancreatic lipase on triglycerides is explained: this enzyme specifically hydrolyses fatty acids esterified with the primary hydroxyl groups of glycerol, forming 2-monoglycerides and free fatty acids. This fact is very important for the further process involving formation and composition of intraluminal micelles, along with absorption and de novo synthesis of triglycerides inside enterocytes. Several different points are disscussed: - Short or medium chain-length fatty acids are hydrolyzed more easily than long-chain ones; after their absorption, the former go to the liver by the portal circulation and the latter go to lymph. - An evaluation of the extent of digestive hydrolysis has been given by means of doubly-labelled triglycerides (glycerol and fatty acids), and by comparing isotope ratio values of lymph and dietary triglycerides. - The physico-chemical state that intraluminal fats are in is discussed; 2-monoglycerides and fatty acids released from triglyceride hydrolysis form macromolecular agregates with biliary salts and phospholipids, cholesterol, and dietary phospholipids (or their degradation products). These are termed mixed micelles and are absorbed by diffusion. - Many recent morphological studies carried out with the electron microscope are indicated. - Two metabolic pathways for triglyceride resynthesis in the mucosal cells have been established, one from free fatty acids and alpha-glycerophosphate, the other from 1 or 2-monoglycerides. Phosphatidic acids are involved in this resynthesis, but the role of other phospholipids is almost certainly not so narrowly limited. - The apparent digestibility of fats according to their fatty acid composition, and mainly according to the location of the fatty acids in the initial triglyceride molecule, is discussed. - The nature and importance of endogenous fatty acids in the digestive tract and lymph is discussed. - The lipid and fatty acid composition of lymph chylomicrons is given. - The importance of lymph lipid particles (average diameter 0,05 less than or equal mum) for transport of exogenous fatty acids is indicated. The biochemical mechanism involved in the digestion and absorption of dietary lipids are now well known, but some processes are still uncertain, particularly the physico-chemical state of intraluminal lipids, the role of enterocyte membranes, the synthesis and secretion of digestive enzymes, and the role of intestinal flora.

Animals↗
PubMed1988

Correction for sample free glycerol is needed for accurate measurement of plasma triglyceride concentrations in miniature Swine.

Methods for the measurement of plasma or serum triglyceride concentrations usually quantify the glycerol released by enzymatic hydrolysis of the triglyceride molecule. Any free glycerol in the sample is measured erroneously as triglyceride in these methods. As miniature swine have been used commonly for comparative studies of plasma lipoprotein lipids, this study was conducted to assess the need for free glycerol correction of plasma triglyceride measurements by comparing glycerol-blank corrected and non-corrected total plasma triglyceride concentrations from fasted minipigs. Fasting plasma free glycerol concentrations range from 9 to 14 mg/dl. The mean +/- SD (n = 16) glycerol-blank corrected total plasma triglyceride value (77 +/- 8 mg/dl) was significantly (p < 0.001) less than the uncorrected measurement value (189 +/- 12 mg/dl). Poor correlation (r = 0.24) between corrected and uncorrected total plasma triglyceride measurements suggests that mathematic correction by a constant correction factor would yield inaccurate results for miniature swine. Free glycerol blanking is essential for determination of the true total plasma triglyceride concentration.

Journal Article↗
PubMed1993

Morphometric analysis demonstrates that metabolically active cardiac triglycerides are 1H NMR visible.

The relationship between myocardial triglyceride content and 1H NMR visible fatty acid resonance intensity was investigated. Hearts from rats fed a 20% rapeseed oil diet contained markedly increased levels of triglycerides as judged by thin layer chromatographic analysis. This elevation in cardiac triglycerides was associated with sharp increases in the cell volume occupied by lipid droplets and in 1H NMR visible fatty acid resonances. Spin-lattice and spin-spin relaxation times of the 1H NMR visible fatty acid resonances from myocardium of rapeseed oil-fed rats were similar in value to those measured for neat triolein. Additionally, the fatty acids constituting these enhanced 1H NMR visible resonances were metabolically active. Perfusion of triglyceride enriched hearts in the presence or absence of glucose caused a time-dependent decrease in the intensity of their 1H NMR visible fatty acid resonances. In contrast, perfusion with glucose+acetate essentially prevented this time-dependent decrease in 1H NMR visible fatty acid resonances. Morphometric analysis of these hearts demonstrated that the decrease in 1H NMR resonance intensity correlated with changes in the cell volume of triglyceride-enriched lipid droplets. These results demonstrate that metabolically active stores of cardiac fatty acids, presumably triglycerides, are 1H NMR visible. Further, they indicate the possible utility of 1H NMR spectroscopy in the future study of myocardial triglyceride metabolism.

Animals↗
PubMed1987

Synthesis, storage and degradation of myocardial triglycerides.

In the mammalian myocardium, an active triglyceride synthesis pathway is operating, (re)esterifying activated fatty acids from endogenous or exogenous sources, with the glycolytically derived three-carbon intermediates dihydroxyacetone-phosphate and glycerol-3-phosphate by the so-called Kennedy pathway. The seven enzymes of triglyceride synthesis are membrane bound and located at the sarcoplasmic reticulum. The first enzyme in the glycerol-3-phosphate pathway, glycerol-3-phosphate acyltransferase, is proposed to be rate limiting for triglyceride formation. This microsomal enzyme is regulated by phosphorylation (inactiycation)-dephosphorylation (activation) coupled to the beta-receptor--adenyl cyclase--protein kinase system. Additional regulatory steps in triglyceride formation are the reactions catalyzed by the microsomal phosphatidic acid phosphatase and diglyceride acyltransferase. Intracellular triglycerides occur as free floating cytosolic droplets, membrane-bound particles and lipid-filled lysosomes. No consensus exists about the metabolically active portion of myocardial triglycerides. Various lipases have been proposed to be involved in endogenous lipolysis: the lysosomal acid, microsomal and soluble neutral triglyceride, intracellular lipoprotein lipases and the microsomal di- and monoglyceridase. It has been acknowledged that the bulk of the intracellular neutral lipase represents the precursor of vascular lipoprotein lipase. The presence of a neutral lipase, as distinct from lipoprotein lipase, in the rat heart was recently advocated. Endogenous lipolysis is a hormone-sensitive process. Hormone-sensitivity may involve direct alteration of enzyme activity by protein phosphorylation-dephosphorylation but is also dependent on the removal rate of product fatty acids, since feedback inhibition is a common property of all lipases in the heart.(ABSTRACT TRUNCATED AT 250 WORDS)

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↗
PubMed1984

Wide variations of plasma triglyceride concentrations in guinea pigs.

Guinea pigs have varying plasma triglyceride concentrations ranging from 28 to 1392 mg/dl, with relatively uniform plasma cholesterol and phospholipid levels. To understand why the animals exhibit such wide variations of plasma triglyceride concentrations, we have explored the triglyceride hydrolyzing system by measuring tissue lipoprotein lipase activities and plasma activator for the enzyme. Lipoprotein lipase activities of epididymal adipose tissue of these animals were 759 +/- 117 (mean +/- SE) n moles FFA X min-1 X g wet tissue-1, markedly low compared with those of rats. There were no relationships between plasma triglyceride concentrations and tissue lipase activities. Plasma activator for lipoprotein lipase was lacking in this animal. Guinea pigs with ascorbic acid deficiency for 2 weeks also showed marked variations of plasma triglyceride concentrations, without any changes in tissue lipoprotein lipase activities. Low adipose tissue lipoprotein lipase activities with deficient plasma activator for the enzyme suggest that the lipoprotein lipase-mediated triglyceride degradation could be impaired in this animal, and this may account for the marked variation of plasma triglyceride concentrations.

Adipose Tissue↗
PubMed1989

Serum fatty acid profiles after intravenous medium chain triglyceride administration.

The serum fatty acid profiles of patients receiving either intravenous medium or long chain triglycerides were studied. Seventeen hospitalized patients, dependent on total parenteral nutrition, were randomly enrolled into a prospective study. The total parenteral nutrition (TPN) delivered amino acids and glucose and either a 75% medium chain triglyceride and 25% long chain triglyceride (MCT group) physical mixture or all long chain triglyceride (LCT group), as the respective fat sources. The amino acids and glucose were given continuously, and the lipid was given for 10 hours each day over five days. Fatty acid profiles on serum triglycerides and free fatty acids were done in the morning before any lipid was given and also later in the afternoon, near the end of the lipid administration, on days 1, 3 and 5. Medium chain fatty acids rose quickly in the triglyceride fraction in patients given MCT. Rapid MCT hydrolysis occurred as evidenced by the appearance of medium chain fatty acids in the free fatty acid fraction in the afternoon sampling. Clearance of the hydrolyzed medium chain free fatty acids (MCFFA) occurred so that little, if any, were present in the morning sampling one day later. Long chain fatty acids, as either triglycerides or free fatty acids, showed expected increases during the daily infusion, but not of such relative magnitude as the medium chain fatty acids. Medium chain fatty acid incorporation into the phospholipid or cholesterol ester fractions by the end of the five-day feeding period was present but minimal.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

Relationship of serum triglyceride concentration to lipoprotein composition and concentration in normolipidemic and hyperlipidemic subjects.

In a series of 438 subjects (184 normolipidemics and 254 hyperlipidemics) the relationship among serum concentration of triglycerides, lipoprotein lipids and apoproteins A-I and B has been evaluated. The results show that as serum triglyceride level increases, VLDL rise and become enriched in triglycerides. The increase of VLDL is associated with a reduction of serum levels of LDL and HDL which appear to be rich in triglycerides and poor in cholesterol. The decrease in serum HDL level is mainly due to a reduction in serum concentration of the HDL2 subfraction. The triglyceride content of HDL2 and HDL3 rises with increasing serum triglycerides. The increase in serum triglyceride concentration seems then to be associated with a complex metabolic derangement which involves all the lipoprotein fractions.

Adolescent↗
PubMed2004

Genome-wide linkage analysis replicates susceptibility locus for fasting plasma triglycerides: NHLBI Family Heart Study.

Recent reports implicate chromosomal regions linked to inter-individual variation in plasma triglycerides. We conducted genome-wide scans to replicate these linkages and/or identify other loci influencing plasma triglycerides in the NHLBI Family Heart Study (FHS). Data were obtained for 501 three-generational families. Genotyping was done by the Utah Molecular Genetics Laboratory and NHLBI Mammalian Genotyping Service; markers from both were placed on one genetic map. Analysis was done using multipoint variance components linkage. Fasting plasma triglycerides were log-transformed and age-, sex-, and field center-adjusted; suggestive linkage evidence was found on chromosome 8 (LOD=2.80 at 89 cM, marker D8S1141). Further adjustment for waist girth, BMI, diabetes, hypertension, and lipid-lowering drugs suggested linkage regions on chromosomes 6 (LOD=2.29 at 79 cM, marker D6S295) and 15 (LOD=1.85 at 43 cM, marker D15S659). Since HDL is correlated with triglycerides and because it was linked to this region on chromosome 15 in FHS, we created a composite triglyceride-HDL phenotype. The combined phenotype LOD score was 3.0 at the same marker on chromosome 15. Chromosome 15 likely harbors a susceptibility locus with an influence on triglycerides and HDL. Regions on chromosomes 6 and 8 may also contain loci contributing to inter-individual variation in plasma triglycerides.

Chromosome Mapping↗