CHO Feeding Research Articles

Preferential Mesenteric Fat Accumulation and Enhanced Portal Free Fatty Acid Delivery in a High-Carbohydrate Diet Fed Rats

The regulation of adipose tissue distribution is an important problem in view of the close epidemiological and metabolic associations between centralized fat accumulation and disease. However, the majority of studies concerning adipose tissue distribution and metabolic disorders have focused on subjects already being obese. In this study, the effects of a high-carbohydrate diet (CHO) and a high-fat diet (FAT) on mass and function of mesenteric adipose depot, drained by the mesenteric vein, was examined in the pre-obese rat model. After 4 weeks of iso-energy feeding, the ratio of mesenteric adipose tissue weight to non-mesenteric was significantly greater in the CHO-fed group than in the FAT-fed group. Incorporation of orally administrated 3H-glucose into the mesenteric depot was more rapid in the CHO-fed group than in the FAT-fed group, but its incorporation into the non-mesenteric depot was similar between the two dietary groups. Arterial and mesenteric concentrations of free fatty acid and triglyceride of the CHO-fed group were significantly higher than those of the FAT-fed group. Gene expression of PPAR-γ and UCP-2 was similar among adipose depots, and there was no significant difference between the two dietary groups. In conclusion, dietary carbohydrate was preferentially incorporated into the total lipid in mesenteric adipose tissue. Without an increase in total body fat, CHO feeding for 4 weeks reinforces incorporation of dietary glucose into mesenteric depot, resulting in an increases of relative mesenteric adipose mass and portal FFA delivery.

EFFECT OF PRE-EXERCISE CARBOHYDRATE FEEDING ON GLYCEMIC AND INSULINEMIC RESPONSES DURING EXERCISE AT DIFFERENT INTENSITIES

Rebound hypoglycemia has been reported after pre-exercise carbohydrate (CHO) ingestion in some studies but not in others. Differences in the experimental design and factors such as the exercise intensity are likely to be responsible for the discrepancies between these studies. Exercise intensity might be a crucial factor since it affects both insulinemia, liver glucose production and muscle glucose uptake. Purpose: Therefore the aim of the present study was to compare the glycemic and insulinemic responses to exercise at different intensities after ingestion of a standardized pre-exercise CHO load. Methods: Eight trained subjects (VO2max 58.4 ± 1.9 ml/kg/min) consumed 75g of glucose 45min prior to 20min of exercise at 55 ± 1, 77 ± 1 and 90 ± 1%VO2max. Blood samples were collected before glucose ingestion, at 15min intervals at rest and 5min intervals during exercise. Results: There were no significant differences in glucose or insulin concentrations between the three trials during exercise. Immediately pre-exercise, plasma glucose concentration had returned to pre-ingestion levels, while the insulin concentration was more than 3 times higher than pre-ingestion (45 ± 10, 62 ± 14, 62 ± 15 vs 16 ± 2, 16 ± 2, 16 ± 1 μU/mL for the 55%, 77% and 90% trials resp.). During exercise, plasma glucose concentration decreased from 4.7 ± 0.3, 5.5 ± 0.3, 4.8 ± 0.3 mmol/L before the start of exercise to 4.1 ± 0.2, 4.0 ± 0.2, 4.1 ± 0.2 mmol/L during the first 5min in the 55%, 77% and 90% trials respectively and then stabilized in all trials. During the 55% and 77% trials, 3 subjects developed hypoglycemia (glucose concentration < 3.5mmol/L), while hypoglycemia occurred in 4 subjects during the 90% trial. Insulin concentrations decreased during the first 10min of exercise and then leveled off at pre-ingestion concentrations. Conclusions: These data suggest that the glycemic response to 75g of CHO 45min pre-exercise is similar during exercise of different intensities. The discrepancies found in studies regarding hypoglycemia after pre-exercise CHO feedings cannot therefore be explained by differences in exercise intensity employed in those studies.

Role of substrate utilization and thermogenesis on body-weight control with particular reference to alcohol.

Alcohol (ethanol; EtOH) provides fuel energy to the body (29.7 kJ (7. 1 kcal)/g, 23.4 kJ (5.6 kcal)/ml), as do other macronutrients, but no associated essential nutrients. The thermogenic effect of EtOH (on average 15 % of its metabolizable value) is much greater than that of the main substrates utilized by the body, i.e. fat and carbohydrates (CHO), suggesting a lower net efficiency of energy utilization for EtOH than for fat and CHO. EtOH cannot be stored in the body and is toxic, so that there is an obligatory continuous oxidation of EtOH and it becomes the priority fuel to be metabolized. In contrast to CHO, its rate of oxidation does not depend on the dose ingested. As with CHO intake, it engenders a shift in postprandial substrate utilization (decrease in fat oxidation), but by a non-insulin-mediated mechanism. A limited amount of EtOH can be converted to fatty acids by hepatic de novo lipogenesis (as occurs with high levels of CHO feeding) from acetate production, which inhibits lipolysis in peripheral tissues. There is no evidence that EtOH consumed under normoenergetic conditions (i.e. isoenergetically replacing CHO or fat) leads to greater body fat storage than fat or CHO. However, there is still a lack of experimental studies on the influence of EtOH on the level of spontaneous physical activity in man. This effect may well depend on the dose of EtOH consumed as well as other intrinsic factors.

Effects of postexercise carbohydrate-protein feedings on muscle glycogen restoration.

The purpose of this investigation was to determine the effects of postexercise eucaloric carbohydrate-protein feedings on muscle glycogen restoration after an exhaustive cycle ergometer exercise bout. Seven male collegiate cyclists [age = 25.6 +/- 1.3 yr, height = 180.9 +/- 3.2 cm, wt = 75.4 +/- 4.0 kg, peak oxygen uptake (VO(2 peak)) = 4.20 +/- 0.2 l/min] performed three trials, each separated by 1 wk: 1) 100% alpha-D-glucose [carbohydrate (CHO)], 2) 70% carbohydrate-20% protein (PRO)-10% fat, and 3) 86% carbohydrate-14% amino acid (AA). All feedings were eucaloric, based on 1.0 g. kg body wt(-1). h(-1) of CHO, and administered every 30 min during a 4-h muscle glycogen restoration period in an 18% wt/vol solution. Muscle biopsies were obtained immediately and 4 h after exercise. Blood samples were drawn immediately after the exercise bout and every 0.5 h for 4 h during the restoration period. Increases in muscle glycogen concentrations for the three feedings (CHO, CHO-PRO, CHO-AA) were 118 mmol/kg dry wt; however, no differences among the feedings were apparent. The serum glucose and insulin responses did not differ throughout the restoration period among the three feedings. These results suggest that muscle glycogen restoration does not appear to be enhanced with the addition of proteins or amino acids to an eucaloric CHO feeding after exhaustive cycle exercise.

Carbohydrate ingestion can completely suppress endogenous glucose production during exercise.

The purposes of this study were 1) to investigate the effect of carbohydrate (CHO) ingestion on endogenous glucose production (EGP) during prolonged exercise, 2) to study whether glucose appearance in the circulation could be a limiting factor for exogenous CHO oxidation, and 3) to investigate whether large CHO feedings can reduce muscle glycogen oxidation during exercise. Six well-trained subjects exercised three times for 120 min at 50% maximum workload while ingesting water (FAST), a 4% glucose solution (LO-Glc), or a 22% glucose solution (HI-Glc). A primed continuous intravenous [6, 6-2H2]glucose infusion was given, and the ingested glucose was enriched with [U-13C]glucose. Glucose ingestion significantly elevated CHO oxidation as well as the rates of appearance (Ra) and disappearance. Ra glucose equaled Ra of glucose in gut (Ra gut) during HI-Glc, whereas EGP was completely suppressed. During LO-Glc, EGP was partially suppressed, whereas Ra gut provided most of the total glucose Ra. We conclude that 1) high rates of CHO ingestion can completely block EGP, 2) Ra gut may be a limiting factor for exogenous CHO oxidation, and 3) muscle glycogen oxidation was not reduced by large glucose feedings.

GLYCEMIC AND INSULINEMIC RESPONSES TO SMALL REPEATED CARBOHYDRATE FEEDINGS BEFORE EXERCISE 1664

Carbohydrate (CHO) feedings in the hour prior to exercise have been shown to result in a relative hypoglycemic response near the onset of the exercise in some cases. This investigation was undertaken to determine whether consuming several small feedings, rather than the traditional single bolus, would alter blood glucose and insulin responses during rest and exercise. Eight trained cyclists ingested either 22.5, 45, or 75 total grams of maltodextrin and dextrose dissolved in 473 ml of water or an equal volume of placebo (PL). Drinks were divided into 4 portions and consumed at 15 min intervals in the hour before a 120 min ride at 65-70% VO2max. Serum glucose values were similarly elevated by each of the CHO feedings at rest, then fell significantly (p<0.05) below baseline and PL at 15 min of exercise. Glucose concentrations immediately prior to exercise (≈5.3 mmol·l-1) and at the 15 min nadir (≈3.2 mmol·l-1) were similar in each of the CHO trials and thus, unrelated to the amount consumed. Insulin concentrations also increased rapidly during rest then fell sharply at the onset of exercise. Total area under the insulin curve was higher in the 75 g trial than both 22.5 g and PL while the 45 g trial exceeded PL. No differences were found in CHO oxidation, perceived exertion or other physiological variables among treatments. At least 2 subjects in each CHO trial expressed subjective feelings of fatigue and exhibited blood glucose values <2.9 mmol·l-1 at 15 min, but all recovered by 30 min and successfully completed the exercise. The conclusion is that CHO consumed during the hour before exercise, even when taken in several small doses, has the potential to produce transient hypoglycemia near the onset of exercise. Additionally, the magnitude of the response appears to be unrelated to the amount of CHO ingested and the insulin concentration.

No effect of carbohydrate feeding on glycogen synthase in human muscle during exercise.

The effect of carbohydrate (CHO) feedings on exercise-mediated changes in glycogen synthase fractional (GSF) activity has been investigated. Subjects cycled at approximately 70% of maximal oxygen uptake on two occasions: the first to fatigue (135 +/- 17 min; mean +/- SE) (control, CON), and the second at the same workload and duration as the first, but with the addition of frequent ingestion of CHO during exercise (0.27 g kg-1 body weight every 15 min). Biopsies were taken from the quadriceps femoris muscle before and immediately after exercise. Plasma glucose and insulin decreased during CON exercise, but remained elevated throughout CHO exercise (end of exercise: glucose = 4.4 +/- 0.2 mM CON vs. 5.8 +/- 0.2 CHO, P < 0.01; insulin = 9 +/- 1 uU ml-1 CON vs. 19 +/- 3 CHO, P < 0.05). Glycogen decreased to approximately 10% of the basal value during CON and to approximately 20% during CHO, and there was no significant difference in net glycogenolysis between treatments. GSF activity averaged 0.25 +/- 0.03 and 0.22 +/- 0.05 at rest, and increased to 0.51 +/- 0.08 and 0.48 +/- 0.09 after exercise in CON and CHO, respectively (P > 0.05 between treatments). It is concluded that under the present conditions CHO feedings do not alter the exercise-mediated changes in GSF activity. The increase in GSF during exercise is attributed at least in part to the decrease in muscle glycogen (which increases the suitability of GS as substrate for GS phosphatase).

Nutritional manipulations before and during endurance exercise

1) Ingesting CHO during prolonged, moderate-intensity (60-85% VO2max) exercise can improve performance by maintaining plasma glucose availability and oxidation during the later stages of exercise. 2) Plasma glucose may be oxidized at rates in excess of 1 g.min-1 late in exercise. Athletes therefore need to ingest sufficient quantities of CHO in order to meet this demand. This can be accomplished by ingesting CHO at 40-75 g.h-1 throughout exercise or by ingesting approximately 200 g of CHO late in exercise. Ingesting CHO after fatigue has already occurred, however, is generally ineffective in restoring and maintaining plasma glucose availability, CHO oxidation, and/or exercise tolerance. 3) No apparent differences exist between glucose, sucrose, or maltodextrins in their ability to improve performance. Ingesting fructose during exercise, however, does not improve performance and may cause gastrointestinal distress. 4) The form of CHO (i.e., solid vs liquid) ingested during exercise is unlikely to be important provided that sufficient water is also consumed when ingesting CHO in solid form. 5) Ingesting 50-200 g of CHO 30-60 min before exercise results in transient hypoglycemia early in exercise, but this does not affect the rate of muscle glycogen utilization or, in most people, cause overt symptoms of neuroglucopenia. Whether performance is impaired, unaffected, or enhanced by such pre-exercise CHO feedings remains equivocal. 6) Ingesting 200-350 g of CHO 3-6 h before exercise appears to improve performance, possibly by maximizing muscle and/or liver glycogen stores or by supplying CHO from the small intestine during exercise itself.(ABSTRACT TRUNCATED AT 250 WORDS)

The effect of an eucaloric high carbohydrate diet on circulating levels of glucose, fructose and non-esterified fatty acids in patients with cirrhosis

Twelve cirrhotic patients and six controls were fed an eucaloric high carbohydrate (CHO) diet for 3 days. Fasting serum triglyceride (TG), non-esterified fatty acids (NEFA), glucose, insulin and glycerol were estimated daily. On the 3rd day of the study we measured NEFA, glucose, insulin, and fructose every 45 min from 07:45 h until 19:45 h, and then every 4 h until 07:45 h the next day. The patients were divided into two groups of six on the basis of plasma lecithin-cholesterol acyltransferase (LCAT) activity: group A cirrhotics (with good liver function--LCAT activity: 40.6-65.7 nmol.ml-1.h-1; mean 48.5), and group B (poor liver function--LCAT: 23.7-32.3; mean 27.4). On the high CHO diet there was an increase in the fasting serum TG with a peak after 2 or 3 days. The increase in serum TG in controls was greater (p less than 0.01) than in either group of cirrhotics. In the controls and in group A most of the extra TG was carried in VLDL; in group B only 39% of the TG increment was found in VLDL. Fasting NEFA fell with 3 days of CHO feeding in the control group (p less than 0.01); they were unchanged in group A, and rose in group B to a significantly higher level than in controls (p less than 0.01). During day 3 when a high CHO diet was fed plasma NEFA levels fell in cirrhotics, and for most of the day the mean NEFA concentration in group B patients was significantly (p less than 0.05) lower than in normals. On day 3 glucose and fructose levels rose after each meal--much more in cirrhotics than in controls (and more in group B than in group A), and for most of the day they were significantly higher in group B patients as compared to the controls (glucose p less than 0.01, fructose p less than 0.001). Our results supported the hypothesis that plasma NEFA would be lower following high CHO meals in cirrhotics than in controls. This suggests that a high NEFA utilisation, which occurs in fasting cirrhotics, is not present throughout the day. Following a CHO meal, we suggest that tissues derive energy directly from the dietary sugars which are present in high concentration during the period of absorption and that this reduces the post prandial requirement for NEFA.

Bilirubin monoglucuronide promotes cholesterol gallstone formation

Recent evidence suggests that cholesterol (Ch) solubility in bile is determined by a complex interaction of mixed micelles and lecithin-cholesterol vesicles. Bilirubin monoglucuronide (BMG), which binds to bile salts and incorporates into mixed micelles, may displace cholesterol from micelles into vesicles, thus favoring cholesterol monohydrate crystal precipitation. Therefore, we designed an experiment to test the hypothesis that BMG may enhance cholesterol gallstone formation without inducing cholesterol supersaturation. For 8 weeks, 28 adult male prairie dogs were fed either a control, nonlithogenic diet (0.03% Ch), a high carbohydrate diet (CHO) which has no cholesterol but increases hepatic bilirubin secretion, or the same CHO diet plus 0.03% Ch. Cholecystectomy was then performed, and bile was examined microscopically for stones or crystals and analyzed for BMG and biliary lipids. Cholesterol saturation index was calculated. Cholesterol gallstones were found in none of the control animals and in 13% of the CHO-fed animals. However, the addition of trace cholesterol to the CHO diet resulted in an 88% incidence of cholesterol gallstones ( P < 0.001 vs control, P < 0.01 vs CHO, respectively). Gallbladder bile was unsaturated with cholesterol in all groups. (control = 0.65 ± 0.05, CHO = 0.46 ± 0.05, CHO + 0.03% Ch = 0.70 ± 0.03). CHO feeding alone or with trace cholesterol significantly elevated gallbladder bilirubin monoglucuronide, phospholipid, and cholesterol concentrations when compared to controls. These data suggest that in the prairie dog a high carbohydrate diet with only trace amounts of cholesterol increases bilirubin monoglucuronide in gallbladder bile and causes cholesterol gallstone formation without inducing cholesterol supersaturation. We conclude that bilirubin monoglucuronide may promote cholesterol precipitation by displacing cholesterol from mixed micelles into lecithin-cholesterol vesicles.

1 Carbohydrate Ingestion During Prolonged Exercise

It is well recognized that energy from CHO oxidation is required to perform prolonged strenuous (greater than 60% VO2 max) exercise. During the past 25 years, the concept has developed that muscle glycogen is the predominant source of CHO energy for strenuous exercise; as a result, the potential energy contribution of blood glucose has been somewhat overlooked. Although during the first hour of exercise at 70-75% VO2max, most of the CHO energy is derived from muscle glycogen, it is clear that the contribution of muscle glycogen decreases over time as muscle glycogen stores become depleted, and that blood glucose uptake and oxidation increase progressively to maintain CHO oxidation (Fig. 1.7). We theorize that over the course of several hours of strenuous exercise (i.e., 3-4 h), blood glucose and muscle glycogen contribute equal amounts of CHO energy, making blood glucose at least as important as muscle glycogen as a CHO source. During the latter stages of exercise, blood glucose can potentially provide all of the CHO energy needed to support exercise at 70-75% VO2max if blood glucose availability is maintained. During prolonged exercise in the fasted state, however, blood glucose concentration often decreases owing to depletion of liver glycogen stores. This relative hypoglycemia, although only occasionally severe enough to result in fatigue from neuroglucopenia, causes fatigue by limiting blood glucose (and therefore total CHO) oxidation. The primary purpose of CHO ingestion during continuous strenuous exercise is to maintain blood glucose concentration and thus CHO oxidation and exercise tolerance during the latter stages of prolonged exercise. CHO feeding throughout continuous exercise does not alter muscle glycogen use. It appears that blood glucose must be supplemented at a rate of approximately 1 g/min late in exercise. Feeding sufficient amounts of CHO 30 minutes before fatigue is as effective as ingesting CHO throughout exercise in maintaining blood glucose availability and CHO oxidation late in exercise. Most persons should not wait, however, until they are fatigued before ingesting CHO, because it appears that glucose entry into the blood does not occur rapidly enough at this time. It also may be advantageous to ingest CHO throughout intermittent or low-intensity exercise rather than toward the end of exercise because of the potential for glycogen synthesis in resting muscle fibers. Finally, CHO ingestion during prolonged strenuous exercise delays by approximately 45 minutes but does not prevent fatigue, suggesting that factors other than CHO availability eventually cause fatigue.

Insulin receptor kinase activity in rat liver. Regulation by fasting and high carbohydrate feeding.

Insulin receptor kinase activity was measured in partially purified receptor preparations from livers of rats fed a standard diet or subjected to either prolonged fasting or a high carbohydrate (CHO) diet, conditions known to decrease (fasting) and increase (CHO) insulin action. Basal and insulin-stimulated phosphorylation of the beta subunit of the insulin receptor was comparable in all groups with a half-maximal effect at approximately 2.0 ng/ml free insulin and a 10-12-fold maximal effect. The kinase activity of insulin receptors from the three groups was further examined using the synthetic polypeptide Glu 4:Tyr 1. Basal and insulin-stimulated rates of Glu 4:Tyr 1 phosphorylation were highest in the CHO-fed and lowest in the fasted group. The magnitude of these differences was the same in the absence or presence of insulin; thus, the alterations in receptor kinase activity in fasting and CHO feeding were entirely expressed in the basal rate of peptide phosphorylation. Antireceptor antibody immunoprecipitated 70-80% of the basal Glu 4:Tyr 1 kinase activity in each group; the remaining 20-30% showed minor group differences when normalized for the amount of protein present in the receptor preparations. These results indicate that the group differences in basal kinase were intrinsic to the insulin receptor. Insulin increased the Vmax of Glu 4:Tyr 1 phosphorylation by approximately 30 fmol of phosphorus/fmol of binding activity/30 min in all three groups; however, the absolute Vmax was highest in the CHO-fed and lowest in the fasted group. The Km of Glu 4:Tyr 1 phosphorylation was unaffected by insulin and was comparable (approximately 0.25 mg/ml) in the three groups. These findings indicate that fasting and CHO feeding produce changes in receptor kinase activity which are regulated by mechanisms independent of insulin and that the alterations show substrate specificity so that differences are detected with one substrate (Glu 4:Tyr 1) but not another (the beta subunit).

Effect of carbohydrate feedings on muscle glycogen utilization and exercise performance

Ten men were studied during 4 h of cycling to determine the effect of solid carbohydrate (CHO) feedings on muscle glycogen utilization and exercise performance. In the experimental trial (E) the subjects ingested 43 g of sucrose in solid form along with 400 ml of water at 0, 1, 2 and 3 h of exercise. During the control trial (C) they received 400 ml of an artificially sweetened drink without solid CHO. No differences in VO2, heart rate, or total energy expenditure were observed between trials; however, respiratory exchange ratios were significantly (P less than 0.05) higher during E. Blood glucose was significantly (P less than 0.05) elevated 20 min post-feeding in E; however, by 50 min no differences were observed between trials until 230 min (E = 4.5 +/- 0.2 mmol X l-1 vs C = 3.9 +/- 0.2, means +/- SE; P less than 0.05). Muscle glycogen utilization was significantly (P less than 0.05) lower during E (100.7 +/- 10.2 mmol X kg-1 w.w.) than C (126.2 +/- 5.5). During a sprint (100% VO2max) ride to exhaustion at the end of each trial, subjects performed 45% longer when fed CHO (E = 126.8 +/- 24.7 s vs C = 87.2 +/- 17.5; P less than 0.05). It was concluded that repeated solid CHO feedings maintain blood glucose levels, reduce muscle glycogen depletion during prolonged exercise, and enhance sprint performance at the end of such activity.

Synergism of thyroid hormone and high carbohydrate diet in the induction of lipogenic enzymes in the rat. Mechanisms and implications.

We have investigated the relationship between the administration of triiodothyronine (T3) and a high carbohydrate (CHO) fat-free diet in the induction of lipogenic enzymes in two rat tissues, liver, and fat. Male thyroidectomized rats were treated with graded daily doses of T3 and either supplemented with a high CHO diet or left on a regular diet. Enzymes studied included malic enzyme (ME), fatty acid synthetase, glucose-6-phosphate dehydrogenase, and 6-phosphogluconate dehydrogenase. In the liver, all four lipogenic enzymes showed a synergistic response between T3 administration and high CHO feeding. In fat, ME also responded synergistically. The interaction was reflected in an increased sensitivity to T3. The dose of T3 required to achieve 50% maximal response was reduced three- to seven-fold by the high CHO diet. This phenomenon could not be attributed to a dietary-induced alteration either in T3 metabolism or in number or affinity of the T3-nuclear receptors. Moreover, studies of the relative rate of synthesis of ME suggested a simultaneous time of onset in the induction of ME, within 2 h after the application of either T3 or CHO. Thus, it is unlikely that either stimulus is secondary to the other. Since parallel experiments from this laboratory (Towle, Mariash, and Oppenheimer,1980. Changes in hepatic levels of messenger ribonucleic acid for malic enzyme during induction by thyroid hormone or diet. Biochemistry. 19: 579-585.) show that ME induction both by CHO and T3 is mediated by an increase in specific messenger RNA for ME, the interaction of T3 and the dietary factor occurs at a pretanslational level.

Carbohydrate Diet-induced Changes in Very Low Density Lipoprotein Composition and Structure

High carbohydrate (CHO) diets cause accumulation in plasma of larger, triglyceride (TG)-enriched very low density lipoprotein (VLDL) particles. In man, the composition of the VLDL is changed by such diets as well. The source of the altered VLDL particles is presumed to be the liver, but the intestine is known to secrete VLDL, and VLDL is also altered during its postsecretory catabolism. To ascertain that the liver is a source of "diet-induced VLDL," we fed rats CHO and control diets and we examined plasma levels of lipids chemically and apoproteins A-I (ApoA-I) and B (ApoB) by specific radioimmunoassay (RIA). VLDL (d less than 1.006) and VLDL density subfractions were isolated and their composition studied by RIA, column chromatography, isoelectric focusing (IEF), and polyacrylamide gel electrophoresis. Livers from control and CHO-fed rats were perfused in vitro. Whole perfusates and perfusate VLDL were studied similary. In the CHO-fed rats, plasma TG increased, cholesterol and ApoA-I remained unchanged, and ApoB fell. The VLDL isolated were TG enriched and less dense. Although total VLDL-protein rose, the proportion of VLDL-protein that was ApoB and arginine-rich protein (ARP) fell, while ApoC rose. The ApoB content varied directly with density of particles. ARP subunits were not changed, but relative proportions of ApoC-III0 rose from 39 to 46 per cent of dye uptake on IEF gels and ApoC-III3 fell from 34 to 26 per cent. Thus, CHO feeding produced altered plasma VLDL in the rat. The perfused livers of the CHO-fed rat secreted more TG, but absolute secretory rates for cholesterol, ApoB, and ApoA-I were unchanged. The VLDL isolated from perfusates were larger, TG-enriched, and less dense. Although VLDL-protein rose, the proportion that was ApoB fell; both ApoC and ARP rose, ARP subunits were unchanged, while ApoC-III0 rose from 29 to 37 per cent and ApoC-III3 fell from 48 to 42 per cent. In contrast to plasma, ApoC content was not increased relative to ARP. As in plasma, content of ApoB varied with particle density. Thus, CHO feeding induced changes in hepatic perfusate VLDL structure and composition that in general paralleled those changes seen in plasma. This strongly suggests that the action of diet on the liver is responsible for many of the changes seen in plasma VLDL. On the other hand, the discrepancy between the VLDL-ApoC content and subunit proportions of plasma and perfusate suggests that the discrepancy is due to postsecretory processing. Similarly, the failure to see decreases in absolute hepatic ApoB secretion, while plasma ApoB levels fell, suggests that the postsecretory metabolism of ApoB-containing lipoproteins is also altered by diet. In addition, the failure to see increases in hepatic VLDL-ApoB secretory rates at a time when VLDL-TG and VLDL-protein increased suggests that there is no tight coupling between the secretion of ApoB and lipids.

The effects of dietary carbohydrate content on insulin binding and glucose metabolism by isolated rat adipocytes.

The effects of changes in the amount of dietary carbohydrate (CHO) on cellular insulin and glucose metabolism have been assessed in rat adipocytes. Feeding animals a 67% CHO (fat-free) diet resulted in decreased insulin binding but enhanced activity of both the glucose transport system and intracellular pathways of glucose metabolism. Feeding rats a 67% fat (CHO-free) diet resulted in decreased insulin receptors as well as decreased activity of the glucose transport system and intracellular glucose metabolism. Therefore, the in vivo insulin resistance caused by a high fat, low CHO diet seems to be adequately explained, since all aspects of insulin's cellular action were depressed. On the other hand, at first approximation, the increased in vivo insulin response caused by a high CHO diet appears contradictory to the observed decrease in insulin binding. However, a probable explanation for this apparent paradox is provided by the enhanced activity of the cellular insulin effector systems distal to the insulin receptor. Therefore, the increased in vivo insulin responsiveness after high CHO feedings is most likely due to post receptor increases in various aspects of glucose metabolism.

SERUM LIPIDS DURING SHORT-TERM HIGH GLUCOSE AND HIGH SUCROSE FEEDING IN INFANTS

The effects of short-term high glucose and high sucrose diets on serum lipids were estimated in six healthy infants aged 4 to 11 months. Each carbohydrate-rich diet was given for 5 days and preceded by 3 days of a "normal" diet. During the high CHO feeding, sucrose or glucose supplied 73% of the total caloric intake, while on the "normal" diet only 40% for the total caloric intake was derived from CHO (glucose only). The percentage of total caloric intake supplied by protein was almost identical in the three diets used. An increase in serum triglyceride (TG) concentration, of almost equal magnitude, was seen following both high CHO feeding periods. Upon resumption of the "normal" diet, serum TG concentrations approached initial concentrations. No consistent changes occurred in total serum cholesterol concentrations or in total serum phospholipid concentrations. A significant increase in the percentage concentration of palmitoleic acid of serum triglyceride fatty acids occurred on both high CHO diets. This increase was slightly but not significantly greater following high sucrose feeding. A significant decrease in the percentage concentration of linoleic acid of serum triglyceride fatty acids occurred on both high CHO diets. This decrease was slightly but not significantly greater following high sucrose feeding. Therefore, it seems that on a short-term basis, high sucrose and high glucose feeding, in healthy infants, will result in similar changes in serum triglyceride concentrations and serum triglyceride fatty acid patterns.