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PubMed1968

Effects of diet on hepatic triglyceride synthesis.

The effects of diet on the rate of triglyceride synthesis by rat liver homogenates was measured. Changes in triglyceride synthesis were correlated with the level of activity of L-alpha-glycerophosphate acyltransferase, the enzyme catalyzing the first specific reaction in hepatic glycerolipid synthesis. Fasting for 48-72 hr depressed the synthesis of triglyceride from L-alpha-glycerophosphate. High carbohydrate diets, fed to rats for 6 days, resulted in increased triglyceride synthesis. Diets high in starch were less effective than high glucose, sucrose, or fructose diets in increasing triglyceride synthesis. Diets high in corn oil did not alter triglyceride synthesis. These studies established the importance of dietary factors in the regulation of hepatic triglyceride synthesis.L-alpha-Glycerophosphate acyltransferase activity was measured after the same dietary changes. Both high carbohydrate and high fat diets resulted in increased enzyme specific activity. Fasting for 72 hr did not decrease activity. Thus, the specific activity of this enzyme did not correlate well with the measured rate of triglyceride synthesis indicating that other factors must participate in the regulation of triglyceride biosynthesis.

Acyltransferases↗

PubMed1988

Interaction of dietary cholesterol and triglycerides in the regulation of hepatic low density lipoprotein transport in the hamster.

These studies report the effects of dietary cholesterol and triglyceride on rates of receptor-dependent and receptor-independent LDL transport in the liver of the hamster. In animals fed diets enriched with 0.1, 0.25, or 1% cholesterol for 1 mo, receptor-dependent LDL transport in the liver was suppressed by 43, 63, and 77%, respectively, and there were reciprocal changes in plasma LDL-cholesterol concentrations. In addition, dietary triglycerides modified the effect of dietary cholesterol on hepatic LDL transport and plasma LDL concentrations so that at each level of cholesterol intake, polyunsaturated triglycerides diminished and saturated triglycerides accentuated the effect of dietary cholesterol. When animals were raised from weaning on diets containing small amounts of cholesterol, the decline in receptor-dependent LDL transport was nearly abolished by the addition of polyunsaturated or monounsaturated triglycerides, but was markedly augmented by the addition of saturated lipids. When animals raised on diets containing cholesterol and saturated triglycerides were returned to the low cholesterol, low triglyceride control diet, hepatic receptor-dependent LDL transport and plasma LDL-cholesterol concentrations returned essentially to normal within 2 wk. Neither receptor-independent LDL transport nor the receptor-dependent uptake of asialofetuin was significantly altered by dietary cholesterol or triglyceride suggesting that the effect of these lipids on hepatic LDL receptor activity was specific and not due to a generalized alteration in the physiochemical properties of hepatic membranes. These studies demonstrate the important role of saturated triglycerides in augmenting the effect of cholesterol in suppressing hepatic LDL receptor activity and elevating LDL-cholesterol levels.

Animals↗

PubMed2003

Squalene synthase inhibitors suppress triglyceride biosynthesis through the farnesol pathway in rat hepatocytes.

We recently demonstrated that squalene synthase (SQS) inhibitors reduce plasma triglyceride through an LDL receptor-independent mechanism in Watanabe heritable hyperlipidemic rabbits (Hiyoshi et al. 2001. Eur. J. Pharmacol. 431: 345-352). The present study deals with the mechanism of the inhibition of triglyceride biosynthesis by the SQS inhibitors ER-27856 and RPR-107393 in rat primary cultured hepatocytes. Atorvastatin, an HMG-CoA reductase inhibitor, had no effect on triglyceride biosynthesis, but reversed the inhibitory effect of the SQS inhibitors. A squalene epoxidase inhibitor, NB-598, affected neither triglyceride biosynthesis nor its inhibition by ER-27856 and RPR-107393. The reduction of triglyceride biosynthesis by ER-27856 and RPR-107393 was potentiated by mevalonolactone supplementation. Treatment of hepatocytes with farnesol and its derivatives reduced triglyceride biosynthesis. In addition, we found that ER-27856 and RPR-107393 significantly reduced the incorporation of [1-(14)C]acetic acid into oleic acid, but not the incorporation of [1-(14)C]oleic acid into triglyceride. Though ER-27856 and RPR-107393 increased mitochondrial fatty acid beta-oxidation, the inhibition of beta-oxidation by RS-etomoxir had little effect on their inhibition of triglyceride biosynthesis. These results suggest that SQS inhibitors reduce triglyceride biosynthesis by suppressing fatty acid biosynthesis via an increase in intracellular farnesol and its derivatives.

Animals↗

PubMed1997

Effects of dietary fructose or glucose on triglyceride production and lipogenic enzyme activities in the liver of Wistar fatty rats, an animal model of NIDDM.

Effects of dietary carbohydrates on triglyceride production and hepatic lipogenic enzyme activities were examined in Wistar fatty rats, an animal model of noninsulin dependent diabetes mellitus, fed fructose or glucose and were compared with those of Wistar lean rats. Carbohydrates were supplied in 10% drinking solutions for 21 days. As compared with lean rats, Wistar fatty rats were characterized by hyperglycemia, hyperinsulinemia and hypertriglyceridemia, the last of which was associated with an increased hepatic activity of fatty acid synthetase and an increased rate of triglyceride secretion from the liver to the circulation. Feeding fructose to genetically obese diabetic rats produced a threefold increase in the hepatic activity of fatty acid synthetase, a twofold increase in NADPH-generating enzymes (malic enzyme and glucose-6-phosphate dehydrogenase) and a 56% increase in the rate of triglyceride secretion, with a resultant 86% increase in plasma triglyceride concentrations. Feeding glucose produced a similar increase in the activity of NADPH-generating enzymes and triglyceride production in the fatty liver but it differed in producing no change in plasma triglyceride concentrations or hepatic fatty acid synthetase activity. Neither dietary fructose nor glucose changed glycemia or insulinemia. These results show that in genetically obese, diabetic rats feeding fructose and glucose is associated with an increase in hepatic lipogenic enzyme activities and triglyceride production, and suggest that fructose stimulates triglyceride production but impairs triglyceride removal, whereas glucose stimulates both of them.

Animals↗

PubMed1990

Triglyceride-rich lipoproteins and atherosclerosis.

Although still the subject of debate, most investigators accept that plasma triglyceride levels are a risk factor for coronary heart disease. Data from epidemiological studies such as the Framingham Heart Study, the Paris Prospective Heart Study and the Stockholm Heart Study have shown that patients with elevated plasma triglyceride levels have a higher incidence of coronary heart disease. In one study, coronary heart disease mortality fell by 36% after continued lowering of plasma triglyceride levels. In patients whose triglyceride levels fell greater than 30%, mortality decreased by 60%. The effect of triglycerides as a risk factor appears to be obscured in studies that use multiple cardiac end-points. Several studies demonstrated a stronger association between plasma triglyceride levels and coronary heart disease in patients with total cholesterol levels less than 5.7 mmol/L, or high density lipoprotein (HDL)-cholesterol levels less than 1 mmol/L. Angiographic data have confirmed these findings and show clearly that elevated triglyceride levels are frequently observed in men with coronary heart disease. Other studies have demonstrated that remnants of triglyceride-rich lipoprotein particles are cytotoxic and atherogenic in vitro and in vivo. Also, patients with familial dys beta-lipoproteinaemia, a condition characterised by high levels of triglyceride-rich very low density lipoprotein (VLDL) particles, have a high risk of atherosclerosis. Thus, there seems to be evidence supporting the atherogenic properties of cholesterylester-rich particles, or remnants thereof.

Arteriosclerosis↗

PubMed2004

Triglycerides induce leptin resistance at the blood-brain barrier.

Obesity is associated with leptin resistance as evidenced by hyperleptinemia. Resistance arises from impaired leptin transport across the blood-brain barrier (BBB), defects in leptin receptor signaling, and blockades in downstream neuronal circuitries. The mediator of this resistance is unknown. Here, we show that milk, for which fats are 98% triglycerides, immediately inhibited leptin transport as assessed with in vivo, in vitro, and in situ models of the BBB. Fat-free milk and intralipid, a source of vegetable triglycerides, were without effect. Both starvation and diet-induced obesity elevated triglycerides and decreased the transport of leptin across the BBB, whereas short-term fasting decreased triglycerides and increased transport. Three of four triglycerides tested intravenously inhibited transport of leptin across the BBB, but their free fatty acid constituents were without effect. Treatment with gemfibrozil, a drug that specifically reduces triglyceride levels, reversed both hypertriglyceridemia and impaired leptin transport. We conclude that triglycerides are an important cause of leptin resistance as mediated by impaired transport across the BBB and suggest that triglyceride-mediated leptin resistance may have evolved as an anti-anorectic mechanism during starvation. Decreasing triglycerides may potentiate the anorectic effect of leptin by enhancing leptin transport across the BBB.

Animals↗

PubMed1996

Interrelationship of triglyceride-rich lipoproteins, serum lipoprotein (a) concentration and apolipoprotein(a) size.

At present, the biochemical mechanisms underlying lipoprotein(a) (Lp(a)) metabolism are not fully understood. We analysed sera from 202 patients with atherosclerotic disease and 109 healthy subjects as a control group to investigate the possible relationship between triglyceride-rich lipoproteins (TRL) and serum lipoprotein(a) levels. To assess the influence of apolipoprotein (apo) (a) isoforms on the Lp(a)-TRL association, the apo(a) phenotypes of 177 patients and 95 controls were included in the analysis. Patients with atherosclerotic disease showed triglyceride levels almost within the normal range. There was no significant correlation between serum Lp(a) levels and triglyceride concentrations, or between Lp(a) and TRL levels in either group. When a subset of subjects from each group with serum triglycerides above 1.7 mmol l-1 was considered, a significant negative correlation between lipid concentration of very low density lipoproteins (VLDL) and serum Lp(a) levels was found only in patients. Control subjects with triglyceride levels under or over 1.7 mmol l-1 showed similar median Lp(a) levels (0.06 gl-1), in contrast to atherosclerotic patients, in whom median Lp(a) concentration was higher in the subset with serum triglycerides under 1.7 mmol l-1 than in those with triglyceride concentration above this value (0.16 vs. 0.13 gl-1). When patients with triglyceride concentrations above 1.7 mmol l-1 were classified into quartiles according to VLDL lipid concentration, subjects with the highest quartiles showed the lowest Lp(a) median levels. Despite the dependence of the Lp(a) concentration on apo(a) size isoforms, we found no effect of apo(a) genetic polymorphism on triglyceride levels or on TRL concentrations. We conclude that the variation in TRL metabolism may constitute a source of variation in serum Lp(a) concentrations that is independent of the genetically determined apo(a) molecule size.

Aged↗

PubMed2003

Hypertriglyceridemia associated with decreased post-heparin plasma hepatic triglyceride lipase activity in hypoxic rats.

Exposure of sated rats to 45% N2 in air for 5h increased serum triglyceride levels by 212% over the levels in normoxic rats. This increase in triglyceride levels was accompanied by a decrease in plasma triglyceride hydrolase activity after intravenous injection of heparin. Further fractionation of the activity by inhibition of lipoprotein lipase indicated that the low triglyceride hydrolase activity is mainly due to a reduction in hepatic triglyceride lipase, which is inversely correlated with the serum triglyceride level. The hypoxic exposure decreased the arterial blood [acetoacetate]/[beta-hydroxybutyrate] ratio in the sated rats, which is believed to reflect the oxidation-reduction state in hepatic mitochondria, but did not affect the level of serum enzymes indicative of tissue damage. On the other hand, triglyceride levels did not change during hypoxic exposure in fasted rats. Thus, hypertriglyceridemia in sated rats following exposure to hypoxia may result from impaired removal of circulating triglycerides by hepatic triglyceride lipase located in the sinusoidal surface of the liver.

Animals↗

PubMed2000

LDL receptor deficiency unmasks altered VLDL triglyceride metabolism in VLDL receptor transgenic and knockout mice.

The very low density lipoprotein receptor (VLDLR) has been proposed to play a role in the delivery of fatty acids to peripheral tissues. However, despite reduced adipose tissue mass in VLDLR-deficient (VLDLR(-)(/-)) mice, this has been difficult to substantiate. In the present study, VLDLR-deficient and VLDLR-overexpressing (PVL) mice were cross-bred onto a low density lipoprotein receptor knockout (LDLR(-)(/-)) background to study the VLDLR under conditions of relatively high serum VLDL and triglyceride levels. Absence of the VLDLR resulted in a significant increase in serum triglyceride levels (1.9-fold) when mice were fed a high fat diet. In contrast, overexpression of the VLDLR resulted in a significant decrease in serum triglyceride levels (2.0-fold) under similar conditions. When kept on a chow diet, a period of prolonged fasting revealed a significant increase in serum triglyceride levels in VLDLR(-)(/-); LDLR(-)(/-) mice (2.3-fold) as compared with LDLR(-)(/-) controls. This could not be attributed to altered apolipoprotein B and VLDL triglyceride production rates. Furthermore, no major differences in nascent VLDL triglyceride content were found between VLDLR(-)(/-); LDLR(-)(/-) mice and LDLR(-)(/-) controls. However, the triglyceride content of circulating VLDL of VLDLR(-)(/-); LDLR(-)(/-) mice (63%) was relatively high as compared with LDLR(-)(/-) controls (49%). These observations suggest that the VLDLR affects peripheral uptake of VLDL triglycerides. In conclusion, under conditions of LDLR deficiency in combination with high fat feeding or prolonged fasting, the effect of the VLDLR on VLDL triglyceride metabolism was revealed.

Animals↗

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

Endotoxin rapidly induces changes in lipid metabolism that produce hypertriglyceridemia: low doses stimulate hepatic triglyceride production while high doses inhibit clearance.

Hyperlipidemia frequently accompanies infectious diseases and may be due to increases in lipoprotein production or decreases in lipoprotein clearance. The administration of endotoxin (LPS) has been used to mimic infection and prior studies demonstrate that LPS produces hypertriglyceridemia. In the present study in rodents, the dose of LPS necessary to induce hyperlipidemia was orders of magnitude less than that necessary to induce shock and death. As little as 10 ng/100 g body weight induced hypertriglyceridemia and this increase in serum triglyceride levels occurred rapidly (78% increase at 2 h). At high doses of LPS (50 micrograms/100 g body weight), the clearance of triglyceride-rich lipoproteins was decreased. At low doses of LPS (100 ng/100 g body weight), triglyceride clearance was not altered but the hepatic secretion of triglyceride was increased. Low dose LPS stimulated hepatic de novo fatty acid synthesis and lipolysis, both of which provided a source of fatty acids for the increase in hepatic triglyceride production. High dose LPS did not increase hepatic fatty acid synthesis or peripheral lipolysis, and hepatic triglyceride secretion was not stimulated. Thus, low dose LPS produces hypertriglyceridemia by increasing hepatic lipoprotein production, while high dose LPS produces hypertriglyceridemia by decreasing lipoprotein catabolism. Administration of anti-tumor necrosis factor (TNF) antibodies or interleukin 1 (IL-1) receptor antagonist did not prevent the increase in serum triglyceride levels induced by LPS. However, anti-TNF antibodies and interleukin 1 receptor antagonist (IL-1ra) blocked the increase in serum triglycerides induced by TNF or IL-1, respectively. These data suggest that neither of these cytokines is absolutely required for the increase in serum triglycerides induced by LPS, raising the possibility that other cytokines, small molecular mediators, or LPS itself may play a crucial role.

Animals↗

PubMed1989

Correlation between apolipoprotein A-IV and triglyceride concentrations in human sera.

Apolipoprotein A-IV concentration was measured by a newly developed competitive enzyme immunoassay in sera from fasted human subjects (n = 105) whose triglyceride concentrations ranged from 20 to 474 mg/dl (total cholesterol below 260 mg/dl) and in which chylomicrons could not be detected. Mean (+/- SD) apolipoprotein A-IV concentration was 13.0 +/- 2.6 mg/dl in sera with triglyceride levels ranging from 20 to 100 mg/dl, 16.9 +/- 3.7 mg/dl in sera with triglyceride levels ranging from 101 to 250 mg/dl, and 22.7 +/- 6.7 mg/dl in sera with triglyceride levels ranging from 251 to 474 mg/dl. The differences among the three groups were highly significant (P less than 0.001). Moreover, variations of apolipoprotein A-IV concentrations according to the triglyceride levels were noted within the normo-triglyceridemic population. Apolipoprotein A-IV concentration was 12.8 +/- 2.1 mg/dl for triglyceride levels ranging from 20 to 75 mg/dl and 16.4 +/- 3.8 mg/dl for triglyceride levels ranging from 76 to 150 mg/dl (P less than 0.01). In the entire population that was studied there was a significant linear correlation (r = 0.61, P less than 0.001) between the concentrations of serum apolipoprotein A-IV and triglyceride. Although the hypothesis of an unknown factor independently influencing both very low density lipoproteins and apolipoprotein A-IV cannot be ruled out, and although no apolipoprotein A-IV was found in the triglyceride-rich lipoprotein fraction after separation by gel filtration, these data suggest that, in fasting subjects, the secretion of very low density lipoproteins could contribute to the plasma apolipoprotein A-IV level.

Adult↗

PubMed1988

Plasma apolipoprotein changes in the triglyceride-rich lipoprotein fraction of human subjects fed a fat-rich meal.

Twenty two subjects (9 males, 13 females) were fed a fat-rich meal (1 g of fat/kg body weight). Triglyceride-rich lipoproteins (TRL) were isolated by ultracentrifugation (d less than 1.006 g/ml) from blood drawn 0, 3, 6, 9, and 12 hr after the meal. Plasma triglyceride increased then decreased postprandially, while plasma apoA-I and apoB concentrations decreased. TRL triglyceride, TRL total protein, and TRL apoB concentrations all increased then decreased after the fat-rich meal. Postprandial rise in plasma triglyceride was significantly correlated with fasting plasma triglyceride levels (r = 0.66, P less than 0.001); postprandial rise in TRL triglyceride was significantly correlated with fasting TRL triglyceride levels (r = 0.58, P less than 0.01); postprandial rise in TRL apoB was not, however, significantly correlated with fasting TRL apoB levels (r = 0.37, N.S.). TRL apolipoproteins were separated by polyacrylamide gradient (4-22.5%) gel electrophoresis and protein bands were scanned in two dimensions with a laser densitometer. Relative postprandial changes in the concentration of the TRL apolipoproteins were determined. TRL apoB-100, apoB-48, apoE, and apoC increased then decreased postprandially. The increase in TRL apoB-100 after the fat-rich meal was confirmed in 8 subjects by direct measurement of apoB-100 with a monoclonal antibody ELISA assay. ApoA-I concentration in TRL was unchanged. Albumin in the TRL fraction was significantly increased 12 hr after the meal. Subjects with a greater magnitude of postprandial triglyceridemia had a greater increase in TRL triglyceride and TRL apoB, but their TRL apoB-100/apoB-48 ratios were not different from subjects with less pronounced triglyceridemia. Assuming that plasma TRL containing apoB-100 are predominantly derived from the liver, our data suggest that triglyceride-rich lipoproteins from both the liver and intestine make a significant contribution to postprandial triglyceridemia.

Adult↗

PubMed1967

Distribution of radioactive glycerol and fatty acids among adipose tissue triglycerides after administration of glucose-U-14C.

Adipose lipid obtained from fed rats 15 or 60 min after injection of radioactive glucose was separated into 10 triglyceride classes of differing fatty acid compositions. The distribution among these classes of total and radioactive triglyceride-glycerol was determined and found to be the same. Thus newly synthesized adipose triglycerides resemble in kind and proportion the triglycerides which exist in the tissue. This finding is in accord with the concept that the structures of adipose triglycerides are stable over long periods and that the turnover rate of the several triglyceride species are similar. After administration of radioactive glucose, the specific activity of saturated fatty acids was higher in the more saturated triglyceride species. These data indicate that newly formed saturated acids do not mix completely with all adipose tissue fatty acids available for esterification. Fatty acids derived from plasma triglyceride influenced the composition of newly synthesized adipose tissue triglyceride and thus constitute an important source of adipose tissue lipid.

Adipose Tissue↗

PubMed1980

The effect of chronic marginal vitamin C deficiency on the rate of secretion and the removal of plasma triglycerides in guinea-pigs.

In guinea-pigs, chronic borderline vitamin C deficiency leads to hypertriglyceridaemia and to the accumulation of triglycerides in the liver. We investigated the triglyceride secretion rate by determining the rate of accumulation of triglycerides in the plasma following a Triton WR 1339 block of the their removal from the plasma (experiment 1) and the rate of the removal of triglycerides from the plasma by mathematical analysis of the specific plasma triglyceride activity - time curve after the administration of 3H-glycerol (experiment 2). In the 14th and 16th week of the experiment it was found that borderline vitamin C deficiency slowed down the triglyceride secretion rate, prolonged the half-time and reduced fractional plasma triglyceride turnover. The balance shift between the rate of the uptake and removal of very low density lipoprotein triglycerides (VLDL-TG) in the plasma compartment (greater retardation of the catabolic phase of kinetics) is probably the reason why triglycerides accumulate in the plasma and liver compartment of guinea-pigs with borderline vitamin C deficiency.

Animals↗

PubMed1984

Effects of alcohol on plasma lipoproteins and cholesterol and triglyceride metabolism in man.

To define the effects of moderate alcohol intake on cholesterol and triglyceride metabolism in man, twelve patients were hospitalized on a metabolic ward and were fed defined diets for 10 weeks. Each patient underwent testing of plasma lipid and lipoprotein levels, of cholesterol metabolism (absorption, fecal excretion, bile saturation), and of triglyceride metabolism [turnover of triglycerides in chylomicrons and very low density lipoproteins (VLDL)]. This testing was done twice, first during a 4-week control period and then during a 4-week period in which 630 calories of alcohol were either added to or substituted for baseline calories. This increased the average baseline caloric intake by only 24% (range 20% to 30% depending on the initial caloric intake). Addition of alcohol to the baseline diet did not cause weight gain in lean individuals. Obese individuals' responses were more variable, and 3/6 definitely gained weight when the diet was supplemented with alcohol. In addition, obese subjects appeared to be more susceptible to the hyperlipidemic effects of alcohol; whereas 4/6 obese patients developed increased total triglyceride and VLDL-triglyceride concentrations when alcohol was administered, concentrations increased with alcohol administration in only 1/6 lean individuals. High density lipoprotein (HDL) cholesterol increased in all volunteers. Low density lipoprotein (LDL) levels did not change. Metabolic studies showed increased transport of VLDL-triglycerides in overweight patients but not in normal weight individuals; increased transport of VLDL-triglycerides in the former was associated with delayed clearance of chylomicron triglycerides. Alcohol consumption did not affect lipoprotein lipase or hepatic triglyceride lipase in six patients in whom these enzyme activities were measured. In the amounts of alcohol taken in this study, no changes were observed in absorption, synthesis, or excretion of bile acids, or percent saturation of gallbladder bile with cholesterol.

Absorption↗

PubMed1980

Regulation of heart triglyceride synthesis in diabetes.

Heart triglyceride content and triglyceride synthesis were studied in control, ketotic diabetic, and insulin-treated rats. Heart triglyceride content was increased in the ketotic diabetic state but was reversed to control values on insulin treatment of the diabetic rats. Triglyceride synthesis in heart homogenates was sensitive to incubation temperature. Triglyceride synthesis from [U-14C]sn-glycero-3-phosphate was increased in the diabetic state, suggesting that increased synthesis played a role in heart triglyceride accumulation. The addition of the end product of triglyceride synthesis, e.g., triolein, to incubation mixtures resulted in inhibition of triglyceride synthesis in heart homogenates of control and diabetic rats. The results suggested that the enzymes of heart triglyceride synthesis were less sensitive to feedback inhibition in the diabetic state.

Animals↗

PubMed1981

The importance of triglyceride hydrolysis for the release of gastric inhibitory polypeptide.

Gastric inhibitory polypeptide is released from the small intestine after the ingestion of fat, but it is not known if triglyceride itself or one of its hydrolytic products is the stimulus to gastric inhibitory polypeptide secretion. Children with cystic fibrosis and defective fat lipolysis were studied to help define the exact stimulus to gastric inhibitory polypeptide secretion. Pancreatic enzyme therapy was withheld from the children with cystic fibrosis during these tests. Ten normal children and 10 children with cystic fibrosis each ingested corn oil and serum immunoreactive gastric inhibitory polypeptide measured. The normal children had a 10-fold increase in serum gastric inhibitory polypeptide levels after the triglyceride, but no increase in immunoreactive gastric inhibitory polypeptide occurred in the children with cystic fibrosis. When three of the children with cystic fibrosis received their pancreatic enzymes and then ingested the triglyceride, gastric inhibitory polypeptide values increased 10-fold. To assess the relative importance of the products of triglyceride hydrolysis and the chain length of the component fatty acids, 6 normal adults consumed, on separate days, 40 mmol of corn oil, medium-chain triglycerides, long-chain fatty acids, or glycerol. Long-chain fatty acids caused a fourfold increase and triglyceride a 12-fold increase in gastric inhibitory polypeptide levels. There was no increase after medium-chain triglyceride or glycerol. This indicates that long-chain fatty acids-the end product of triglyceride hydrolysis-are a stimulus to gastric inhibitory polypeptide secretion; that this release is apparently proportional to the quanitity of long-chain fatty acid present; and that hydrolysis of triglyceride is required before gastric inhibitory polypeptide release can normally occur after fat ingestion.

Adolescent↗