Changes in blood lipids during six days of overfeeding with medium or long chain triglycerides

Although medium chain triglyceride (MCT) is less calorically dense than long chain triglyceride (LCT), it produces a greater thermic effect following ingestion. We hypothesized that the previously observed high rate of thermogenesis produced by MCT overfeeding was due to hepatic de novo synthesis of long chain fatty acids (LCFA) from the excess medium chain fatty acids (MCFA). To study this, we compared the effects of overfeeding MCT- and LCT-containing diets on blood lipid profiles. Ten in-patient, nonobese males were overfed (150% of estimated energy requirements) two formula diets for 6 days each, in a randomized crossover design. Diets differed only in the composition of the fat and contained either 40% of energy as MCT or LCT (soybean oil). The major differences between diets in the resulting pattern of blood lipids were: 1) a reduction in fasting serum total cholesterol concentrations with the LCT, but not the MCT diet; and 2) a threefold increase in fasting serum triglyceride concentrations with MCT, but not LCT, diet. Moreover, 10% of the fasting triglyceride fatty acids were medium chain and 40% were 16:0 with the MCT diet. This compared to 1% and 20% for medium chain and 16:0, respectively, with the LCT diet. In addition, there were increases in 16:1, 18:0, and 18:1 in the triglycerides during MCT feeding. The changes in fatty acids in triglycerides with MCT feeding are consistent with the hypothesis that excess dietary MCT cause a significant increase in the hepatic synthesis of these fatty acids from MCFA through de novo synthesis and/or chain elongation and desaturation. These processes could account for the higher rate of postprandial thermogenesis with MCT as compared to LCT.     

Plasma fatty acids and [13C]linoleic acid metabolism in preterm infants fed a formula with medium-chain triglycerides

Most preterm infant formulas contain medium-chain triacylglycerols (MCT), but the effects of MCT on polyunsaturated fatty acid status and metabolism are controversial. Thus, we studied the effects of MCT on linoleic acid metabolism using stable isotopes. Enterally fed preterm infants were randomized to receive for 7 days 40% of fat as MCT (n = 10) or a formula without MCT (n = 9). At study day 5, infants received orally 2 mg/kg body weight of (13)C-labeled linoleic acid. Fatty acids in plasma lipid classes and (13)C enrichment of phospholipid fatty acids were measured and tracer oxidation was monitored. Compared with the control group, the MCT group showed lower breath (13)CO(2) and higher plasma triacylglycerol contents of octanoic acid, of decanoic acid, and of total long-chain polyunsaturated fatty acids (57.1 +/- 4.4 micro mol/l vs. 37.9 +/- 4.8 micro mol/l, P < 0.01). Concentrations of several polyunsaturated fatty acids in plasma phospholipids and non esterified fatty acids were higher in the MCT group. (13)C concentrations in phospholipid n-6 fatty acids indicated no difference in the relative conversion of linoleic to arachidonic acid. We conclude that oral MCT effectively reduce polyunsaturated fatty acid and long chain polyunsaturated fatty acid oxidation in preterm infants without compromising endogenous n-6 long chain polyunsaturated fatty acid synthesis.     

Impaired pancreatic polypeptide response to insulin hypoglycemia in obese subjects

We have studied the effect of insulin hypoglycemia on the secretion of pancreatic polypeptide (PP) in 14 obese subjects with normal glucose tolerance and in 6 normal controls. Infusion of insulin 0.1 U/kg/h in controls and 0.12 U/kg/h in the obese, for one hour, produced a progressive hypoglycemia, similar in both groups (nadir 2 mmol/l at 50 min). The secretion of PP was less in obese subjects than in controls (peak 116 mmol/l vs 184 pmol/l, P less than 0.01) (integrated secretion sigma delta PP 288 vs 472 pmol/l, P less than 0.01) and was also delayed in the obese subjects beginning at 50 min instead of 40 min. The secretion of glucagon and of C-peptide were not different in the two groups, but the integrated response of ACTH was higher in the obese (sigma delta ACTH 52 pmol/l vs 25 pmol/l, P less than 0.01). The secretory response of growth hormone (STH) was smaller in the obese group (peak 8.6 +/- 1.28 vs 21.4 +/- 6.4 ng/ml, P less than 0.01). The reduced secretion of PP in obese subjects could be due to impaired sensitivity to hypoglycemia of the central control mechanism for PP release. The similarity of the reductions in the secretion of both PP and STH support this hypothesis, although a reduction in the secretory capacity of pancreatic PP cells cannot be excluded.     

The effect of atropine on bombesin and gastrin releasing peptide stimulated gastrin, pancreatic polypeptide and neurotensin release in man

The effects of 1-h infusions of bombesin and gastrin releasing peptide (GRP) at 50 pmol/kg per h and neurotensin at 100 pmol/kg per h on gastrin, pancreatic polypeptide (PP) and neurotensin release in man were determined following either saline or atropine infusion (20 micrograms/kg). Bombesin produced a rise in plasma neurotensin from 32 +/- 6 to 61 +/- 19 pmol/l and of PP from 26 +/- 8 to 36 +/- 7 pmol/l. There was a further rise of plasma PP to 50 +/- 13 pmol/l after cessation of the infusion. GRP had no significant effect on plasma neurotensin, but compared to bombesin, produced a significantly greater rise in plasma PP from 34 +/- 6 to 66 +/- 19 pmol/l during infusion. There was no post-infusional increase. At this dose, GRP was as effective as bombesin in releasing gastrin, although unlike bombesin its effect was enhanced by atropine. Neurotensin produced a rise in plasma PP from 17 +/- 4 to 38 +/- 8 pmol/l. Atropine blocked the release of PP during GRP and neurotensin infusion. Atropine had no effect on neurotensin or PP release during bombesin infusion, but did block the rise in plasma PP following bombesin infusion. We conclude that, in contrast to meal-stimulated neurotensin release, bombesin-stimulated neurotensin release is cholinergic independent. Despite structural homology, bombesin and GRP at the dose used are dissimilar in man in their actions and sensitivity to cholinergic blockade.     

A high-fat diet enriched in medium chain triglycerides triggers hepatic thermogenesis and improves metabolic health in lean and obese mice

Obesity, liver steatosis and type 2 diabetes are major diseases partly imputed to energy-dense diets rich in long chain triglycerides (LCT). The search for bioactive nutrients that help to overcome metabolic diseases is a growing field. In this regard, medium chain triglycerides (MCT) were shown to promote lipid catabolism and to stimulate brown adipose tissue thermogenesis. The objective of our study was to evaluate if the replacement of LCT by MCT in high-fat diets could prevent and/or reduce metabolic disorders. For this purpose, two cohorts of C57BL/6 mice were fed during 10 weeks with three isocaloric high-fat diets with variable MCT content. Cohort A was composed of lean mice while cohort B was composed of obese, insulin resistant mice. In cohort A, replacement of LCT by MCT preserved metabolic health, in part by triggering hepatic thermogenesis. We further found that medium chain fatty acids promote thermogenesis markers within cultured hepatocytes in a FFAR1/GPR40-dependent manner. In cohort B, high-fat diets enriched in MCT promoted body fat depletion and caused metabolic health improvement, together with the induction of thermogenesis markers in the liver as well as in subcutaneous white adipose tissue. Our study supports that replacement of LCT by MCT in high-fat diets improves the metabolic features associated with obesity.     

Effect of fatty acid chain length on suppression of ghrelin and stimulation of PYY, GLP-2 and PP secretion in healthy men

We have evaluated the effects of fatty acid chain length on ghrelin, peptide YY (PYY), glucagon-like peptide-2 (GLP-2) and pancreatic polypeptide (PP) secretion and hypothesized that intraduodenal administration of dodecanoic ("C12"), but not decanoic ("C10"), acid would decrease plasma ghrelin and increase PYY, GLP-2 and PP concentrations. Plasma hormone concentrations were measured in seven healthy men during 90-min intraduodenal infusions of: (i) C12, (ii) C10 or (iii) control (rate: 2 ml/min, 0.375 kcal/min for C12/C10) and after a buffet-meal consumed following the infusion. C12 markedly suppressed plasma ghrelin and increased both PYY and GLP-2 (all P < 0.05) compared with control and C10, while C10 had no effect. Both C10 and C12 increased PP concentrations slightly (P < 0.05). We conclude that the effects of intraduodenal fatty acids on ghrelin, PYY and GLP-2 secretion are dependent on their chain length.     

Metabolic effects of intravenous LCT or MCT/LCT lipid emulsions in preterm infants

Most lipid emulsions for parenteral feeding of premature infants are based on long-chain triacylglycerols (LCTs), but inclusion of medium-chain triacylglycerols (MCTs) might provide a more readily oxidizable energy source. The influence of these emulsions on fatty acid composition and metabolism was studied in 12 premature neonates, who were randomly assigned to an LCT emulsion (control) or an emulsion with a mixture of MCT and LCT (1:1). On study day 7, all infants received [13C]linoleic (LA) and [13C]alpha-linolenic acid (ALA) tracers orally. Plasma phospholipid (PL) and triacylglycerol (TG) fatty acid composition and 13C enrichments of plasma PL fatty acids were determined on day 8. After 8 days of lipid infusion, plasma TGs in the MCT/LCT group had higher contents of C8:0 (0.50 +/- 0.60% vs. 0.10 +/- 0.12%; means +/- SD) and C10:0 (0.66 +/- 0.51% vs. 0.15 +/- 0.17%) than controls. LA content of plasma PLs was slightly lower in the MCT/LCT group (16.47 +/- 1.16% vs. 18.57 +/- 2.09%), whereas long-chain polyunsaturated derivatives (LC-PUFAs) of LA and ALA tended to be higher. The tracer distributions between precursors and products (LC-PUFAs) were not significantly different between groups. Both lipid emulsions achieve similar plasma essential fatty acid (EFA) contents and similar proportional conversion of EFAs to LC-PUFAs. The MCT/LCT emulsion seems to protect EFAs and LC-PUFAs from beta-oxidation.     

Omega-3 long-chain fatty acids strongly induce angiopoietin-like 4 in humans

Angiopoietin-like 4 (ANGPTL4) is a regulator of LPL activity. In this study we examined whether different fatty acids have a differential effect on plasma ANGPTL4 levels during hyperinsulinemia in healthy lean males. In 10 healthy lean males, 3 hyperinsulinemic euglycemic clamps were performed during concomitant 6 h intravenous infusion of soybean oil (Intralipid® rich in PUFA), olive oil (Clinoleic® rich in MUFA) and control saline. In 10 other healthy lean males, 2 hyperinsulinemic clamps were performed during infusion of a mixed lipid emulsion containing a mixture of fish oil (FO), medium-chain triglycerides (MCTs), and long-chain triglycerides (LCTs) (FO/MCT/LCT; SMOFlipid®) or saline. FFA levels of approximately 0.5 mmol/l were reached during each lipid infusion. Plasma ANGPTL4 decreased during hyperinsulinemia by 32% (18–52%) from baseline. This insulin-mediated decrease in ANGPTL4 concentrations was partially reduced during concomitant infusion of olive oil and completely blunted during concomitant infusion of soybean oil and FO/MCT/LCT. The reduction in insulin sensitivity was similar between all lipid infusions. In accordance, incubation of rat hepatoma cells with the polyunsaturated fatty acid C22:6 increased ANGPTL4 expression by 70-fold, compared with 27-fold by the polyunsaturated fatty acid C18:2, and 15-fold by the monounsaturated fatty acid C18:1. These results suggest that ANGPTL4 is strongly regulated by fatty acids in humans, and is also dependent on the type of fatty acid.     

Physiological plasma concentrations of cholecystokinin stimulate pancreatic enzyme secretion and gallbladder contraction in man

The present study was undertaken to determine whether infusion of cholecystokinin (CCK) to plasma concentrations comparable to those found after a meal stimulates pancreatic enzyme secretion and gallbladder contraction. Plasma CCK concentrations were measured by radioimmunoassay using antibody T204, which binds to all carboxyl-terminal CCK-peptides containing the sulfated tyrosine region. Ingestion of a standardized test meal in 7 normal subjects induced significant increases in plasma CCK from 2.0 +/- 0.2 pmol/l to levels between 4.6 +/- 0.6 and 7.3 +/- 1.0 pmol/l (p less than 0.05-p less than 0.0005). Infusion of 2.5 pmol/kg X h CCK 33 resulted in significant increases in plasma CCK from 2.0 +/- 0.2 to 3.9 +/- 0.3 pmol/l (p less than 0.0005). This infusion of CCK induced significant increases in trypsin secretion from 0.5 +/- 0.1 to 1.4 +/- 0.2 KU/15 min (p less than 0.005) and in bilirubin output from 1.6 +/- 0.7 to 30.3 +/- 8.0 mumol/15 min (p less than 0.05). It is concluded that physiological plasma concentrations of CCK stimulate pancreatic enzyme secretion and gallbladder contraction in man.     

Heparin-modulated binding of pancreatic lipase and uptake of hydrolyzed triglycerides in the intestine

Utilizing small intestine membranes that contain heparin (50 micrograms/mg protein), binding of triglyceride lipase (homogeneous 52 kDa, specific activity, 70 nmol/mg.h) to membranes was shown to be concentration dependent and saturable, and it was characterized by a single dissociation constant (KD = 86 +/- 16 nM) with a maximal binding capacity of 54 +/- 8 pmol/mg of vesicle protein. Specific binding was decreased in a concentration-dependent manner by the addition of exogenous heparin, and binding was virtually eliminated (less than 6% control values) by pretreatment of membranes with bacterial heparinase. Cultured intestinal epithelial cells (CaCo-2), shown to possess membrane-associated heparin, also bound pancreatic triglyceride lipase in a specific and saturable manner, with KD = 77 +/- 12 nM and Bmax = 13.7 +/- 6 pmol/10(6) cells. Soluble heparin not only decreased binding, but it also diminished the enzyme-mediated cellular uptake of [14C]oleate from [14C]triolein by over 75%. Therefore, intestinal heparin, a component of the brush border membrane, localizes pancreatic triglyceride lipase in a receptor-like manner to the plasma membrane to promote the subsequent absorption of fatty acids derived from hydrolyzed triglycerides.     

Inhibition of muscular ketone extraction by lipid infusion in man

Using the forearm technique, muscular ketone body metabolism was investigated in 12 healthy volunteers during an i.v. infusion of lipid emulsions containing long chain triglycerides (LCT) or a mixture of medium- and long chain triglycerides (MCT/LCT). During the basal period, arterial concentrations and muscular extraction of beta-hydroxybutyrate and acetoacetate were linearly correlated as expected. This relationship was abolished during the infusion of both lipid emulsions. In addition, fractional extraction rates of ketone bodies were reduced. These changes were most probably mediated by elevated levels of free fatty acids and triglycerides as well.     

Effect of immunoneutralisation of cholecystokinin on bombesin-stimulated pancreatic enzyme secretion in the rat

Infusion of bombesin stimulates plasma cholecystokinin (CCK) and pancreatic enzyme secretion in various species, including the rat. This study was undertaken in two groups of four conscious rats with a cannulated pancreatic duct to determine the role of endogenously released CCK in mediating the effect of bombesin on pancreatic enzyme secretion. Infusion of 2 ml CCK antiserum or normal rabbit serum for 40 min was followed 10 min later by infusion of 18 pmol/kg bombesin for 30 min and after an interval of 90 min by infusion of 24 pmol/kg CCK for 30 min. After administration of control rabbit serum, pancreatic protein secretion increased by 3.2 +/- 1.0 mg/30 min during bombesin and 4.0 +/- 1.5 mg/30 min during CCK, while the plasma CCK increments were 1.7 +/- 0.5 pM and 7.0 +/- 0.9 pM for the bombesin and CCK infusions, respectively. Immunoneutralisation with the CCK antiserum did not significantly affect bombesin-stimulated pancreatic protein secretion (3.6 +/- 1.3 mg/30 min), but almost abolished the pancreatic protein response to CCK (0.5 +/- 0.2 mg/30 min). It is therefore concluded that CCK is not an important mediator of the stimulatory effect of bombesin on the pancreas in the rat.     

Transesterification reaction between medium- and long-chain fatty acid triglycerides using surfactant-modified lipase

Transesterification between medium-chain fatty acid triglycerides (MCT) and long-chain fatty acid triglycerides (LCT) in a nonsolvent system was investigated using surfactant modified lipase which is a complex of lipase, Rhizopus japonicus and surfactant, sorbitan monostearate. 74% conversion of was obtained after a 48-h reaction period, and the triglyceride composition was well described by the 1, 3-random 2-random stochastic model. The transesterification reaction between MCT and LCT closely followed the simple kinetic model, and the change in MCT and LCT contents could be simulated using one parameter. The effects of the water activity (A(w)) of modified lipase, the water content of the reaction system and the reaction temperature on the reaction rate were studied. A modified lipase A(w) of 0.35 and a water content of the reaction system at 0.09 wt % showed the highest activity. Inactivation did not occur below 60 degrees C, however, the activity decreased at temperatures over 70 degrees C.     

Maternal plasma triglycerides as a source of fetal fatty acids.

The transfer of plasma triglyceride fatty acids from mother to fetus was studied in rats. Following i.v. injection of labelled chylomicron and very low density lipoprotein (VLDL) triglycerides into the mother, the time courses of the plasma triglycerides, free fatty acids, and fetal radioactivity were determined. The data were analysed using a mathematical model. From the results the following conclusions were drawn: To cover the need of fetal fatty acids, the placenta utilizes only VLDL triglycerides but not chylomicron triglycerides. Comparison of the amount of VLDL triglyceride fatty acids (0.04 micromoles/min/litter) and of maternal plasma free fatty acids (0.08 micronmoles/min/litter) transferred into the fetus indicates that the maternal plasma triglycerides are a source of fetal fatty acids, that cannot be neglected.     

Acute inhibition of lipolysis does not affect postprandial suppression of endogenous glucose production

To test the hypothesis that intrahepatic availability of fatty acid could modify the rate of suppression of endogenous glucose production (EGP), acipimox or placebo was administered before and during a test meal. We used a modified isotopic methodology to measure EGP in 11 healthy subjects, and (1)H magnetic resonance spectroscopic measurement of hepatic triglyceride stores was also undertaken. Acipimox suppressed plasma free fatty acids markedly before the meal (0.05 +/- 0.01 mmol/l at -10 min, P = 0) and throughout the postprandial period (0.03 +/- 0.01 mmol/l at 150 min). Mean peak plasma glucose was significantly lower after the meal on acipimox days (8.9 +/- 0.4 vs. 10.1 +/- 0.5 mmol/l, P < 0.01), as was mean peak serum insulin (653.1 +/- 99.9 vs. 909 +/- 118 pmol/l, P < 0.01). Fasting EGP was similar (11.15 +/- 0.58 micromol.kg(-1).min(-1) placebo vs. 11.17 +/- 0.89 mg.kg(-1).min(-1) acipimox). The rate of suppression of EGP after the meal was almost identical on the 2 test days (4.36 +/- 1.52 vs. 3.69 +/- 1.21 micromol.kg(-1).min(-1) at 40 min). There was a significant negative correlation between the acipimox-induced decrease in peak plasma glucose and liver triglyceride content (r = -0.827, P = 0.002), suggesting that, when levels of liver fat were low, inhibition of lipolysis was able to affect glucose homeostasis. Acute pharmacological sequestration of fatty acids in triglyceride stores improves postprandial glucose homeostasis without effect on the immediate postprandial suppression of EGP.     

Effect of somatostatin infusion on VIP-induced transport changes in the human jejunum

This study was designed to elucidate the mechanism by which somatostatin administration ameliorates or abolishes diarrhea in pancreatic cholera syndrome (PCS). Absorption (or secretion) of water and electrolytes was measured in 30-cm segments of jejunum of 18 healthy volunteers in whom PCS was mimicked by intravenous infusion of VIP. Using the triple-lumen tube technique, the intestine was perfused with a plasma-like electrolyte solution while administering intravenous saline (control), VIP (400 pmol/kg/hr), somatostatin (5000 pmol/kg/hr), or VIP plus somatostatin. VIP infusion abolished water and electrolyte absorption and somatostatin had no effect on these VIP-induced transport changes regardless of whether somatostatin infusion was started before or after VIP infusion. Somatostatin infusion had no effect on VIP plasma concentration when elevated by intravenous VIP infusion (control: 10 +/- 1 pmol/l; during VIP infusion: 108 +/- 6). In a patient with pancreatic cholera syndrome identical perfusion experiments showed jejunal water secretion (93 ml/30 cm/hr) which changed to absorption (65 ml/30 cm/hr) when somatostatin was infused (5000 pmol/kg/hr). Plasma VIP concentration fell from 145 to 74 pmol/l (normal less than 50) during somatostatin infusion. Stool weight fell from 3722 g to 819 g per 24 hours when somatostatin was given at a dose of 2500 pmol/kg/hr for two days. Our observations in healthy subjects show that somatostatin has no effect on intestinal transport at the mucosal level when circulating VIP concentration is elevated.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of medium-chain triglycerides on the postprandial triglyceride concentration in healthy men

This study compared the serum lipid concentrations after a single dose of medium-chain triglycerides (MCT) or long-chain triglycerides (LCT) between individuals grouped according to the body mass index (BMI). Twenty-five males participated as volunteers, the test diet containing 10 g of MCT or LCT. Blood samples were collected up to 6 h after the intake of a test diets. The LCT diet resulted in significantly greater increases in areas under the curves (AUCs) for serum and chylomicron triglyceride in the BMI > or = 23 kg/m2 group than those in the BMI < 23 kg/m2 group. The magnitude of response after intake of the MCT diet by the BMI > or = 23 kg/m2 group was significantly lower than that after the LCT diet. These results suggest that, in subjects with BMI > or = 23 kg/m2, the intake of MCT is preferable to that of LCT for maintaining postprandial triglyceride at a low concentration.     

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.     

Aging is associated with myocardial insulin resistance and mitochondrial dysfunction

Aging is associated with insulin resistance, often attributable to obesity and inactivity. Recent evidence suggests that skeletal muscle insulin resistance in aging is associated with mitochondrial alterations. Whether this is true of the senescent myocardium is unknown. Twelve young (Y, 4 years old) and 12 old (O, 11 years old) dogs, matched for body mass, were instrumented with left-ventricular pressure gauges, aortic and coronary sinus catheters, and flow probes on left circumflex artery. Before surgery, all dogs participated in a 6-wk exercise program. Dogs underwent measurements of hemodynamics and plasma substrates before and during a 2-h hyperinsulinemic-euglycemic clamp to measure whole body and myocardial glucose and nonesterified fatty acid uptake. Following the protocol, myocardial and skeletal samples were obtained to measure components of the insulin-signaling cascade and mitochondrial structure. There was no difference in plasma glucose (Y, 90 +/- 4 mg/dl; O, 87 +/- 4 mg/dl), but old dogs had higher (P < 0.02) nonesterified fatty acids (Y, 384 +/- 48 micromol/l; O, 952 +/- 97 micromol/l) and plasma insulin (Y, 39 +/- 11 pmol/l; O, 108 +/- 18 pmol/l). Old dogs had impaired total body glucose disposition (Y, 11.5 +/- 1 mg x kg(-1) x min(-1); O, 8.0 +/- 0.5 mg x kg(-1) x min(-1); P < 0.05) and insulin-stimulated myocardial glucose uptake (Y, 3.5 +/- 0.3 mg x min(-1) x g(-1); O, 1.8 +/- 0.3 mg x min(-1) x g(-1); P < 0.05). The impaired insulin action was associated with altered insulin signaling and glucose transporter (GLUT4) translocation. There were myocardial mitochondrial structural changes observed in association with decreased expression of uncoupling protein-3. Aging is associated with both whole body and myocardial insulin resistance, independent of obesity and inactivity, but involving altered mitochondrial structure and impaired cellular insulin action.     

Absorption of triglycerides in the absence of lipase

Medium chain triglycerides are considered to be readily absorbed intact in the absence of pancreatic lipase, unlike long chain triglycerides. Commercial medium chain triglyceride oils comprise various medium chain fatty acids from 6 to 12 carbons in length resulting in triglyceride molecules of different sizes and molecular weights. The effect of molecular weight and hence fatty acid chain length on the efficiency of intact medium chain triglyceride absorption is unknown. Therefore, this study measured, using a single-pass marker perfusion technique, intestinal jejunum absorption of five medium chain and one long chain triglycerides in anesthetized Sprague-Dawley rats. The molecular weights of the five medium chain triglycerides were 470.7, 498.8, 526.8, 554.9, 639.0, and the long chain triglyceride, 885.4. Residual luminal pancreatic lipase was removed prior to lipid perfusion. This study demonstrated that medium chain triglycerides were absorbed in the absence of lipase whereas long chain triglyceride was not. There was no significant variation in the absorption of the five different medium chain triglycerides perfused. The molecular weight of the medium chain triglyceride did not affect its intact absorption by the small intestine.