Increase In FFA Research Articles

STRESS RESPONSE TO A 50K NORDIC SKI RACE

PURPOSE: Cross-country ski racing requires use of nearly all of the body's muscle mass. There is very limited information on the physiologic responses to exhaustive cross country ski-racing in the elite athletes. Marathon racing has been described in terms of the stress response(Nieman et al 1989). Therfore the purpose of the study was to examine the leukocyte and hormonal responses to a 50K World Cup SKI-race and compare them to studies where a lower % of total muscle mass is involved. METHODS: 10 elite male crosscountry skiers(age23–32 years, VO2max 81–92ml/kg/min)were recrutied. They followed usual pre-race routines. During the 50K race all the athletes drank 1.0–1–5 L of CHO-electrolyte sports drink. Venous blood samples were taken pre and immeditaly post race. Wilcoxon's signed rank test was used for statistical analysis. RESULTS: From pre race to post race numbers of leukocytes (3X), granulocytes (5X), lympohocytes, NK cells (1.5X), B-cells were significantly increased. Hemoglobin monocytes, CD3+, CD4+, and CD8+ cells were unchanged. Significant increases in EPI (10X, NE (5X), cort (2X), GH (22X), GLU (1.5X), and FFA (3X) were observed. Testosterone levels were unchanged while insulin concentration decreased. In comparsion to changes observed in marathon racing (an event of similar duration), the changes in this study were 2 or 3 times as great. CONCLUSIONS: There is an extremeky lagre stress of response to a 50K cross country ski race which is substantially greater than that observed in marathon running. We speculate that this is due to the greater % of total muscle mass involved in cross-country skiing.

Effects of Phosphate Injection on Metabolic and Hormonal Responses to Exercise in Fructose-Injected Rats

GHANBARI–NIAKI, A., F. DÉSY AND J.-M. LAVOIE. Effects of phosphate injection on metabolic and hormonal responses to exercise in fructose-injected rats. PHYSIOL BEHAV 67(5) 747–752, 1999.—The purpose of the present study was to evaluate the effects of an intraperitoneal injection of sodium phosphate on the metabolic and hormonal responses to exercise. Fructose-injected rats were either injected with sodium phosphate (Na 2HPO 4) or NaCl, either in a fed or in a food-restricted state (24 h), and evaluated at rest or after a 30-min exercise period (26 m/min; 0% grade). Liver ATP, phosphate (Pi), and glycogen concentrations were, on the whole, significantly ( p < 0.05) higher in Na 2HPO 4 than in NaCl groups. Exercise resulted in a significant ( p < 0.01) decrease in liver ATP and glycogen levels in fed and food-restricted rats whether injected with NaCl or Na 2HPO 4. Exercise, after NaCl and Na 2HPO 4 injection, resulted in a significant ( p < 0.01) increase in liver phosphate and Pi/ATP ratio, and in a decrease in glucose and an increase in glucagon levels in food-restricted rats only. The normal exercise-induced increase in plasma FFA, glycerol, and norepinephrine levels ( p < 0.05), observed in both fed and food-restricted NaCl-injected rats, was abolished by the injection of phosphate. The data are in line with the new concept that in addition to blood glucose levels, the increase in liver Pi/ATP ratio could also contribute to the increase in glucagon response during exercise.

Free fatty acids (FFA), a link between obesity and insulin resistance.

Evidence, gained from human studies, is reviewed showing that elevation of plasma FFA levels produce peripheral and probably also hepatic insulin resistance in obese healthy and diabetic subjects. First, plasma FFA levels are elevated in most obese subjects. Second, physiological elevations of plasma FFA inhibit acutely as well as chronically insulin stimulated glucose uptake in a dose dependent fashion. Responsible for this inhibition is a FFA induced defect in insulin stimulated glucose transport and/or phosphorylation which develops after 3-4 hours of raising plasma FFA and a second defect, consisting of inhibition of glycogen synthase, the rate limiting enzyme of glycogen synthesis, which develops after 4-6 hours. FFA induced inhibition of fatty acid oxidation (Randle effect) does not affect insulin stimulated glucose uptake or glycogen synthesis and thus does not cause insulin resistance. Elevated plasma FFA levels also modestly increase insulin suppressed endogenous glucose production (EGP) although this effect has not been found by all investigators. The reasons why it has been difficult to demonstrate unequivocal effects of FFA on EGP include 1) the fact that FFA promote insulin secretion which counteracts its effect on EGP (FFA increase, while insulin decreases EGP); 2) the recognition that FFA induced increase in gluconeogenesis may be compensated by intrahepatic downregulation of EGP (i.e., by a decrease in glycogenolysis). The FFA induced insulin resistance is physiologically important during starvation by preserving carbohydrate for oxidation in the central nervous system and during pregnancy, where the well recognized accelerated starvation pattern provides carbohydrate for the growing fetus. In obesity, however, there is no need to spare carbohydrate and the FFA induced insulin resistance may result in type 2 diabetes and other cardiovascular risk factors.

Demonstration of a critical role for free fatty acids in mediating counterregulatory stimulation of gluconeogenesis and suppression of glucose utilization in humans.

In vitro studies indicate that FFA compete with glucose as an oxidative fuel in muscle and, in addition, stimulate gluconeogenesis in liver. During counterregulation of hypoglycemia, plasma FFA increase and this is associated with an increase in glucose production and a suppression of glucose utilization. To test the hypothesis that FFA mediate changes in glucose metabolism that occur during counterregulation, we examined the effects of acipimox, an inhibitor of lipolysis, on glucose production and utilization ([3-3H]glucose), and incorporation of [U-14C]-alanine into glucose during insulin-induced hypoglycemia. Eight normal volunteers were infused with insulin for 8 h to produce modest hypoglycemia (approximately 3 mM) on two occasions, first without acipimox (control) and then with acipimox administration (250 mg per os at 60 and 240 min). Despite identical plasma insulin concentrations, glucose had to be infused in the acipimox experiments (glucose-clamp technique) to maintain plasma glucose concentrations identical to those in control experiments. Acipimox completely prevented counterregulatory increases in lipolysis so that during the last 4 h plasma FFA were below baseline values and averaged 67 +/- 13 vs. 725 +/- 65 microM in control experiments, P < 0.001. Concomitantly, overall glucose production was reduced by 40% (5.5 +/- 11 vs. 9.3 +/- 0.7 mumol/kg per min, P < 0.001), and gluconeogenesis from alanine was reduced by nearly 70% (0.32 +/- 0.09 vs. 1.00 +/- 0.18 mumol/kg per min, P < 0.001), while glucose utilization increased by 15% (10.8 +/- 1.4 vs. 9.3 +/- 0.7 mumol/kg per min). We conclude that FFA play a critical role in mediating changes in glucose metabolism during counterregulation, and that under these conditions, FFA exert a much more profound effect on hepatic glucose production than on glucose utilization.

Stimulation of the binding properties of adult rat corticosteroid- binding globulin by a lipolysis-induced rise in plasma free fatty acids

In vitro studies have shown that FFA induce conformational changes in human corticosteroid-binding globulin (CBG). We increased the plasma FFA concentrations of adult male rats by injecting heparin to determine whether such changes in CBG binding and immunological properties also occur in vivo. The in vivo transient activation of lipase by heparin produced a large increase in plasma FFA at 10 and 20 min (P < 0.01), which was maximal at 60 min (P < 0.005) and remained elevated at 120 min (P < 0.01) postinjection. This rise in FFA was associated with a 2- to 3-fold increase in the binding indices (C values; liters per g) of corticosterone (B) and progesterone to CBG 60-120 min postinjection (P < 0.001). There was a good positive correlation (r = 0.85) between the increase in B binding and the rise in plasma FFA in heparin-treated rats. The enhanced B binding to CBG resulted from a 2-fold increase in the apparent number of binding sites, without any significant change in the affinity constant (Ka). FFA extracted from postheparin plasma and a standard FFA mixture induced similar changes in B binding to purified mature rat CBG. The immunological behavior of CBG was not significantly changed after heparin-induced lipolysis, but the immunoreactivity of CBG from heparin-treated rats was more reduced by incubation with exogenous FFA than that from controls. FFA extracted from the plasma of heparin-treated rats and a standard FFA mixture both produced a dose-dependent drop in the immunodetection of pure CBG. These binding and immunological studies indicate that FFA mediate conformational changes in rat CBG in vivo. Thus, FFA, in addition to their roles as metabolic energy sources and components of complex lipids, can be rapid potent endogenous modulators of steroid-protein interactions.

Stimulation of the binding properties of adult rat corticosteroid-binding globulin by a lipolysis-induced rise in plasma free fatty acids.

In vitro studies have shown that FFA induce conformational changes in human corticosteroid-binding globulin (CBG). We increased the plasma FFA concentrations of adult male rats by injecting heparin to determine whether such changes in CBG binding and immunological properties also occur in vivo. The in vivo transient activation of lipase by heparin produced a large increase in plasma FFA at 10 and 20 min (P < 0.01), which was maximal at 60 min (P < 0.005) and remained elevated at 120 min (P < 0.01) postinjection. This rise in FFA was associated with a 2- to 3-fold increase in the binding indices (C values; liters per g) of corticosterone (B) and progesterone to CBG 60-120 min postinjection (P < 0.001). There was a good positive correlation (r = 0.85) between the increase in B binding and the rise in plasma FFA in heparin-treated rats. The enhanced B binding to CBG resulted from a 2-fold increase in the apparent number of binding sites, without any significant change in the affinity constant (Ka). FFA extracted from postheparin plasma and a standard FFA mixture induced similar changes in B binding to purified mature rat CBG. The immunological behavior of CBG was not significantly changed after heparin-induced lipolysis, but the immunoreactivity of CBG from heparin-treated rats was more reduced by incubation with exogenous FFA than that from controls. FFA extracted from the plasma of heparin-treated rats and a standard FFA mixture both produced a dose-dependent drop in the immunodetection of pure CBG. These binding and immunological studies indicate that FFA mediate conformational changes in rat CBG in vivo. Thus, FFA, in addition to their roles as metabolic energy sources and components of complex lipids, can be rapid potent endogenous modulators of steroid-protein interactions.

Glucagon does not increase plasma free fatty acid and glycerol concentrations in patients with noninsulin-dependent diabetes mellitus.

The study was initiated to determine whether physiological elevations of plasma glucagon would increase plasma FFA or glycerol concentrations in patients with noninsulin-dependent diabetes mellitus (NIDDM). To do this, patients were infused for 6 h with somatostatin (SRIF) alone or with SRIF plus glucagon. Furthermore, these studies were performed with an insulin infusion rate that maintains basal insulin levels or without any insulin infusion. Infusion of SRIF alone was associated with an increase in plasma FFA and glycerol concentrations, whereas hepatic glucose production and plasma glucose concentrations fell somewhat. When glucagon was added to SRIF, plasma FFA and glycerol concentrations were again increased, but to a significantly lesser extent. In addition, the addition of glucagon was associated with a modest increase in hepatic plasma glucose production and plasma glucose concentrations. In contrast, plasma FFA and glycerol concentrations fell when SRIF was infused in the presence of basal insulin levels. The decrease in FFA and glycerol levels tended to be accentuated when glucagon was also infused. It should be noted that the increases in hepatic glucose production and plasma glucose concentration after glucagon was added to SRIF were prevented when basal insulin levels were replaced. These results demonstrate that an increase in the plasma glucagon level comparable to that seen in patients with NIDDM was associated with lower, not higher, plasma FFA and glycerol concentrations in patients with NIDDM. Furthermore, these changes were seen in the absence of insulin or when basal insulin levels were replaced. Thus, the higher ambient plasma FFA and glycerol concentrations in patients with NIDDM do not appear to be secondary to increased plasma glucagon levels.

Alternative extraction effects on the free fatty acids and phosph in oil from damaged and undamaged soybeans

By varying the extracting conditions, it may be possible to produce high‐quality, low‐phosphorus and low‐free fatty acid (FFA) oil extracted from water or mechanically damaged soybeans. The variability in phospholipids and FFA was studied in oil extracted by an alternative process from undamaged, damaged and aged soybeans subjected to various changes. Forrest and Hutcheson cultivars were used, and extractions were from finely ground flour rather than from flakes. Freezing caused the maximum increase in FFA and phosphorus levels compared to other levels in damaged or undamaged soybeans, but the levels were reasonable compared to flake extraction. Phosphorus and FFA increased when storage temperatures went from 25 to 45°C, extraction temperatures from 25 to 50°C and moisture of the flour from 6 to 10%. However, the storage time of soybeans with initially high moisture (20%) did not have a marked influence on FFA and phosphorus levels. Immediately after grinding moisture of the flour elevated or lowered the phosphorus level to a great extent, although it had little influence on the FFA level. Phosphatidic acid and phosphatidylcholine were identified as the main phospholipids present when total phosphorus was low in extracted oil. The time taken for the flour to dry to 6% moisture (after grinding and before it was extracted) was critical. The alternative extraction process moderated the expected increase in FFA and phospholipids as the result of soybean damage.

Effects of a physiological growth hormone pulse on substrate metabolism in insulin-dependent (type 1) diabetic subjects.

When present in inappropriate amounts GH induces substantial insulin resistance and it has furthermore been suggested that modest nocturnal surges of GH may precipitate the emergence of the dawn phenomenon. To characterize the metabolic effects of physiologically relevant, small-scale GH exposure, six type 1 diabetic subjects were studied for 5 h in the postabsorptive state after an iv pulse of either 210 micrograms GH or saline. Identical amounts of insulin were infused on both occasions to maintain a prevailing blood glucose concentration of 125 +/- 12 mg/100 ml. The GH bolus caused an increase in serum GH levels to a peak value of 22 +/- 2 micrograms/L after 10 min, a 70% increase in serum FFA (from 570 +/- 80 to 980 +/- 60 mumol/L) and a 400% increase in blood 3-hydroxybutyrate (3-OHB) (from 100 +/- 15 to 420 +/- 35 mumol/l) concentrations after 180 and 240 min respectively (P less than 0.05). Blood glycerol and forearm uptake of 3-OHB rose in parallel (P less than 0.01). Plasma glucose, isotopically measured glucose turnover and forearm glucose uptake was not affected by GH. Blood lactate concentrations increased (P less than 0.05) and nonoxidative glucose use and lipid oxidation tended to increase with GH. Energy expenditure remained unaffected. These results suggest that under everyday conditions GH acts as an important regulator of fuel fluxes in type 1 diabetic subjects, the main effect being a transient stimulation of lipolysis. Since no significant effect on glucose metabolism was recorded, we do not presently find evidence to support a primary role for small surges of GH in the pathogenesis of the dawn phenomenon.

Effect of acute acidosis and alkalosis on leucine kinetics in man.

The effects of acute pH changes on whole body leucine kinetics (1-13C-leucine infusion technique) were determined in normal subjects. Plasma insulin, glucagon, and growth hormone concentrations were kept constant by somatostatin and replacement infusions of the three hormones. When acidosis was produced by ingestion of NH4Cl (4 mmol kg-1 p.os; n = 8) arterialized pH decreased within 3 h from 7.39 +/- 0.01 to 7.31 +/- 0.01 (P less than 0.001) and leucine plasma appearance increased by 0.13 +/- 0.04 mumol kg-1 min-1 (P less than 0.02); in contrast, when alkalosis was produced by intravenous infusion of 4 mmol kg-1 NaHCO3 (n = 7, pH 7.47 +/- 0.01), leucine plasma appearance decreased by -0.09 +/- 0.04 mumol kg-1 min-1 (P less than 0.01 vs. acidosis). Whole body leucine flux also increased during acidosis compared to alkalosis (P less than 0.05), suggesting an increase in whole body protein breakdown during acidosis. Apparent leucine oxidation increased during acidosis compared to alkalosis (P = 0.05). Net forearm leucine exchange remained unaffected by acute pH changes. Plasma FFA concentrations decreased during acidosis by -107 +/- 67 mumol l-1 (P less than 0.05) and plasma glucose increased by 1.90 +/- 0.25 mmol l-1 (P less than 0.02); in contrast, alkalosis resulted in an increase in plasma FFA by 83 +/- 40 mumol l-1 (P less than 0.02; P less than 0.01 vs. acidosis), suggesting an increase in lipolysis; plasma glucose decreased compared to acidosis (P less than 0.01). The data demonstrate that acute metabolic acidosis and alkalosis, as they occur in clinical conditions, influence protein breakdown, and in the opposite direction, lipolysis.

Effect of exercise on recovery changes in plasma levels of FFA, glycerol, glucose and catecholamines

The prolonged effects of acute exercise on the plasma concentrations of FFA, glycerol, glucose and catecholamines were examined. Twelve young men performed exhaustive prolonged exercise on a cycle ergometer (80 minutes at 70-75% of VO2 max), and in separate experiments they exercised for shorter durations (20, 40 and 80 minutes) and at lesser intensities (29, 50 and 75% of VO2 max). Carbohydrate-rich meals were given 2, 7 and 12 hours after exercise. Blood samples were taken while the subjects rested in bed during a 12-14-hour recovery period. Control experiments without exercise were also performed. In some subjects the plasma concentration of FFA after exhaustive exercise was increased to levels considered to be potentially hazardous, and the mean plasma level of FFA was increased for 6 hours and that of glycerol was increased for 2.5 hours after exercise. The plasma concentration of glucose was generally reduced for 12 hours after exhaustive exercise. Plasma catecholamines were increased for 2 hours after exhaustive exercise. We observed a preprandial increase in FFA and glycerol concentrations during recovery from exercise which was related to the duration and intensity of exercise. These findings indicate that the rates of FA utilization and TG-FA substrate cycling were increased in the recovery period after exercise, and that the magnitude of both depends on the duration and intensity of exercise.

Short time effects of growth hormone on glucose metabolism and insulin and glucagon secretion in normal man

The present study was undertaken in order to evaluate the acute metabolic and hormonal effects of human growth hormone in healthy subjects. Glucose turnover, plasma glucose, FFA, insulin, C-peptide, glucagon, and somatostatin concentrations were determined in the fasting state after a bolus injection of placebo or growth hormone in quantities producing increases in plasma growth hormone levels within the normal physiological range. We found that growth hormone administration resulted in negligible changes in plasma glucose, no significant changes in appearance or disappearance rates of glucose, a moderate increase in FFA and a moderate fall in plasma insulin, C-peptide and glucagon concentrations, while plasma somatostatin levels were unchanged. These findings suggest that rapid changes in plasma growth hormone concentrations, corresponding to the fluctuations seen during normal daily life, may play a role in the short time regulation of blood glucose concentration through an inhibition of insulin and glucagon secretion.

Desensitization of β-Receptor Mediated Responses to Epinephrine in Fetal Lambs by Prolonged Ritodrine Administration

During prolonged administration of beta-agonists such as ritodrine directly to chronically cannulated fetal lambs, the cardiovascular, metabolic, and endocrine changes observed during the 1st day of administration, lessen and return to normal within 3-4 d despite continuing drug administration. In our investigation, heart rate, plasma FFA, lactate, glucose, and insulin concentrations all increased significantly during the 1st day of ritodrine infusion (10 micrograms/min), whereas blood PO2 and base excess were significantly decreased. After 3 d, despite continued drug infusion, all these changes had ameliorated. To examine the hypothesis that this tachyphylaxis to ritodrine also results in decreased sensitivity to endogenous catecholamines, epinephrine (1 microgram/min i.v. for 60 min, then 2 micrograms/min i.v. for a further 60 min) was infused into fetal lambs (124-130 d gestation) 1 d before, then 5 +/- 1 d after, and again 10 +/- 1 d after beginning ritodrine infusion. Before ritodrine administration, epinephrine significantly increased plasma FFA, lactate, glucose, and glucagon concentrations and decreased insulin. However, after ritodrine treatment for either 5 +/- 1 or 10 +/- 1 d, epinephrine resulted in no significant increases in FFA or glucagon, and those in lactate and glucose were significantly reduced. Decreases in insulin during epinephrine administration were unchanged by ritodrine. Initial responses of mean arterial pressure and heart rate to epinephrine were significantly greater during prolonged ritodrine treatment. Fetal responses to epinephrine mediated through beta-adrenergic receptor mechanisms were clearly decreased when administration of beta-agonists was prolonged beyond 24 h.

Mechanism of the heparin-induced increase in the concentration of free thyroxine in plasma.

The iv administration of heparin causes an increase in the plasma free T4 concentration, as determined by equilibrium dialysis. The mechanism and physiological consequences of this action of heparin are unknown. To explore the possibility that the heparin-induced increase in plasma free T4 is an in vitro artifact due to generation of FFA during equilibrium dialysis, we studied plasma samples from 10 subjects treated with iv heparin. In plasma from 4 of these subjects, free T4 concentrations measured by equilibrium dialysis did not increase above baseline values after heparin administration. In incubations performed in parallel with the equilibrium dialysis measurements, FFA concentrations in these plasma samples were found to increase, but in no subject did they exceed 2.5 meq/L after incubation. In contrast, in plasma from the other 6 subjects treated with heparin, free T4 concentrations rose markedly (by 130-520%) above baseline values after heparin administration. In all of these postheparin plasma samples, FFA concentrations were less than 2.8 meq/L before incubation, but rose during incubation by 80-270% to more than 3.8 meq/L. Treatment of these plasma samples with protamine to inhibit lipoprotein lipase and with specific antiserum to inhibit hepatic triglyceride lipase before equilibrium dialysis or incubation prevented, in parallel, the heparin-induced increases in FFA and free T4 concentrations. From these findings we conclude that the heparin-induced increase in free T4 is usually an in vitro artifact, and that most subjects receiving heparin have a normal plasma free T4 concentration in vivo. We also conclude that this in vitro artifact may account for many of the findings that led to the postulate of an inhibitor of T4 binding to plasma and intracellular proteins in heparin-treated patients and perhaps in patients with nonthyroid illness as well.

Free fatty acids block growth hormone (GH) releasing hormone-stimulated GH secretion in man directly at the pituitary.

Increases in plasma FFA levels inhibit GH responses to a variety of pharmacological and physiological stimuli. To gain further insight into the mechanism by which FFA exert their effect, we studied the plasma GH responses to GHRH-(1-44) (1 microgram/kg, iv) in normal subjects in whom plasma FFA levels were raised by a lipid-heparin infusion (250 mL 10% Intralipid plus 2500 U heparin). Paired tests were performed in 10 normal subjects, with and without lipid-heparin pretreatment. Lipid-heparin infusion from -30 to 120 min increased mean FFA levels from 0.41 +/- 0.03 (+/- SEM) to 3.12 +/- 0.40 mmol/L at 120 min. The mean plasma GH levels after GHRH administration were lower at all times; however, the values were significantly different (P less than 0.05) only at the later times (45, 60, and 90 min). When considered individually, an all or none pattern was observed; 5 subjects had no plasma GH response to GHRH, and 5 had no reduction. To investigate the time relationships between the FFA peak and subsequent GH blockade, a different protocol of paired tests was performed with GHRH with or without a different lipid-heparin infusion protocol. Lipid-heparin was infused from -90 to 0 min, with an additional heparin pulse at -15 min, to obtain a higher and earlier (0 min) FFA increase. FFA increased from 1.06 +/- 0.19 to 11.61 +/- 0.83 mmol/L at zero time. The GHRH-induced GH secretory peak (15.8 +/- 3.5 ng/ml) at 15 min was completely blocked (0.9 +/- 0.2 ng/ml), and the mean plasma GH levels were also lower at 30, 45, and 60 min. To determine whether the FFA-induced blockade of GH secretion was exerted in the pituitary, a series of in vitro studies was conducted using monolayer cultures of rat anterior pituitary glands, with GHRH concentrations of both 10(-10) and 10(-8) M and 10(-5) M forskolin to stimulate GH release. Both caprylic and oleic acid inhibited basal GH release and GHRH- or forskolin-induced GH release. PRL release was not altered, nor were toxic actions noted on the cells. In conclusion, FFA are able to block GH secretion directly at the pituitary level.

Chemical and fungal evaluation of graded sunflowerseed

AbstractThirty‐four samples of commercial oil‐type sunflower‐seed graded No. 1, 10 samples graded No. 2 and 33 samples graded Sample grade (SG) were used to study the relationship between percent heat damage, an important grading character, and percent FFA, percent color and UV absorption of extracted oil, percent germination and number and identities of fungi present. Seventy‐two fungal species belonging to 28 genera were isolated. Thirty‐seven fungal species in 17 genera were isolated from grade No. 1 seed; 68 species in 13 genera were isolated from grade No. 2 seed, and 68 species in 26 genera were isolated from SG seed. The genera most frequently isolated from grade No. 1 seed wereAlternaria (85.3%),Phoma (4.7%) andCladosporium (4.5%).Alternaria alternata was recovered from all No. 1 samples and comprised 75.6% of all isolates. The genera most frequently isolated from grade No. 2 seed wereAlternaria (74.5%),Eurotium (8.4%) andPhoma (7.7%). Fewer fungal species were isolated from grade No. 2 than from No. 1 seed, but a greater recovery of storage fungi was found for No. 2 seed (13.3%) than for No. 1 seed (2.5%).Alternaria (33.8%),Eurotium (33.1%) andMicroascus (8.3%) were the genera most frequently isolated from SG seed. Species of common storage fungi (Eurotium, Microascus, Penicillium andAspergillus) were recovered more frequently from SG than from Grades No. 1 and No. 2. In general, as the quality of the seed decreased from grade No. 1 to grade No. 2 to SG, there was an increase in percent heat damage, percent FFA, Lovibond color and UV absorption of extracted oil, and a decrease in percent germination. Analysis of variance of the quality characteristics data showed no significant differences between grade No. 1 and No. 2 seed except for UV 228 nm absorption. However, the quality characteristics of SG seed all differed significantly from those of grades No. 1 and No. 2 seed with the exception of percent seed yielding fungi. Correlation coefficients of the quality characteristics of SG showed a slight relationship between heat damage and percent FFA (r=0.63) and UV 228 nm absorbance (r=0.68). Although many of the SG seed were badly heat damaged, no statistical relationship was found between percent heat damage and percent seed yielding fungi or total isolates of storage fungi. The data in this study show that errors exist in grading decisions when seed are judged visually to be heat damaged.

Haemorheologic and lipidemic parameters in obesity and diabetes

Haemorheologic and lipidemic tests were performed in 3 groups of children: 20 with obesity (14m,6f., age 11.4±2.6y) defined as a weight excess of at least 20% (OC) ; 16 with type 1 diabetes in compensated phase (7m.,9f.,age 11.9±2.OY) (DC) ; and 20 normal children (15m.,5f.,age 11.9±2,1y.) (NC). For haemorheologic tests by analysis of variation the 3 groups were significantly different for blood viscosity (BV,p<0,01 for both 230 and 23/sec-1), plasma viscosity (PV,p<0,01) and fibrinogen (Fg,p<0,01), but not for haematocrit (HT) and erythrocyte filtration time (1ml.20% erythrocyte suspension in autologous plasma, EFT). The differences were entirely due to OC and not to DC:BV 230 sec. was cP 4.63± 0.46 in OC versus 4.19±0.30 in NC (p<0.005); PV was cP 1.66± 0.08 in OC vs. 1.55±0.08 in NC (p<0.001); and FG was mg% 341± 53 in OC vs. 254±82 in NC (p<0.001) for lipidemic tests, OC had significantly increased triglycerides (p<0.05), FFA (p<0.05) but not cholesterol, and significantly lowered Lipoprotein (p<0.01). DC differed from normals only for increase in FFA (p<0.01). These data show that early haemorheologic changes, esp. in hyper Fg and increased PV and DV are observed in childhood obesity rather than in juvenile diabetes. These changes do not involve EFT, in either condition. The chronic metabolic disorder due to obesity affects the lipidemic profile much more than type 1 diabetes.

Interactions between glucagon and other counterregulatory hormones during normoglycemic and hypoglycemic exercise in dogs.

Somatostatin (ST)-induced glucagon suppression results in hypoglycemia during rest and exercise. To further delineate the role of glucagon and interactions between glucagon and the catecholamines during exercise, we compensated for the counterregulatory responses to hypoglycemia with glucose replacement. Five dogs were run (100 m/min, 12 degrees) during exercise alone, exercise plus ST infusion (0.5 micrograms/kg-min), or exercise plus. ST plus glucose replacement (3.5 mg/kg-min) to maintain euglycemia. During exercise alone there was a maximum increase in immunoreactive glucagon (IRG), epinephrine (E), norepinephrine (NE), FFA, and lactate (L) of 306 +/- 147 pg/ml, 360 +/- 80 pg/ml, 443 +/- 140 pg/ml, 541 +/- 173 mu eq/liter, and 6.3 +/- 0.7 mg/dl, respectively. Immunoreactive insulin (IRI) decreased by 10.2 +/- 4 micro/ml and cortisol (C) increased only slightly (2.1 +/- 0.3 micrograms/dl). The rates of glucose production (Ra) and glucose uptake (Rd) rose markedly by 6.6 +/- 2.2 mg/kg-min and 6.2 +/- 1.5 mg/kg-min. In contrast, when ST was given during exercise, IRG fell transiently by 130 +/- 20 pg/ml, Ra rose by only 3.6 +/- 0.5 mg/kg-min, and plasma glucose decreased by 29 +/- 6 mg/dl. The decrease in IRI was no different than with exercise alone (10.2 +/- 2.0 microU/ml). As plasma glucose fell, C, FFA, and L rose excessively to peaks of 5.4 +/- 1.3 micrograms/dl, 1,166 +/- 182 mu eq/liter and 15.5 +/- 7.0 mg/dl. The peak increment in E (765 +/- 287 pg/ml) coincided with the nadir in plasma glucose and was four times greater than during normoglycemic exercise. Hypoglycemia did not affect the rise in NE. The increase in Rd was attenuated and reached a peak of only 3.7 +/- 0.8 mg/kg-min. During glucose replacement, IRG decreased by 109 +/- 30 pg/ml and the IRI response did not differ from the response to normal exercise. Ra rose minimally by 1.5 +/- 0.3 mg/kg-min. The changes in E, C, Rd, and L were restored to normal, whereas the FFA response remained excessive. In all protocols increments in Ra were directly correlated to the IRG/IRI molar ratio while no correlation could be demonstrated between epinephrine or norepinephrine and Ra. In conclusion, (a) glucagon controlled approximately 70% of the increase of Ra during exercise. This became evident when counterregulatory responses to hypoglycemia (E and C) were obviated by glucose replacement; (b) increments in Ra were strongly correlated to the IRG/IRI molar ratio but not the plasma catecholamine concentration; (c) the main role of E in hypoglycemia was to limit glucose uptake by the muscle; (d) with glucagon suppression, glucose production was deficient but a further decline of glucose was prevented through the peripheral effects of E, (e) the hypoglycemic stimulus for E secretion was facilitated by exercise; and (f) we hypothesize that an important role of glucagons during exercise could be to spare muscle glycogen by stimulating glucose production by the liver.

Comparison of carbohydrate and lipid metabolism in mice and rats during fasting

1. 1. Swiss albino mice and Sprague-Dawley derived rats, 6–8 weeks in age were compared in the fed condition and after a fast of 24 and 48 hr. 2. 2. Plasma glucose was significantly higher in mice than rats in the fed state but this difference disappeared after the 48 hr fast. 3. 3. In the fed condition, plasma FFA and glycerol levels were significantly higher in mice than rats yet did not change during fasting. With starvation, there was a progressive increase in plasma FFA in the rat but no change in plasma glycerol. 4. 4. The content of triacylglycerols in the plasma and liver was comparable in mice and rats in the fed state. Plasma triacylglycerols declined to a similar extent in both species during a fast of 48 hr. In mice, hepatic triacylglycerols increased markedly during fasting but declined in rats. 5. 5. Heart triacylglycerols were higher in mice than rats in the fed state and increased still further during a fast of 48 hr during which time little change was observed in the rat. Myocardial glycogen was comparable in mice and rats in the fed state. With fasting, cardiac glycogen content decreased in the mouse but remained unchanged in the rat. 6. 6. Distinct differences in certain of the parameters of carbohydrate and lipid metabolism were found with mice and rats in the fed and fasted condition.

Pathophysiology of metabolic acidosis: effect of low pH on the hepatic uptake of lactate, pyruvate and alanine.

The uptake of lactate, pyruvate and alanine in perfused rat liver was investigated under normal perfusion conditions (pH 7.4, PCO2 40 mmHg) and under conditions mimicking partially compensated metabolic acidosis (pH 6.9, PCO2 20 mmHg). At 1 mM lactate as well as 10 mM lactate in the medium a lowering of pH from 7.4 to 6.9 did not affect the lactate plus pyruvate uptake. A significant effect of the low pH was seen on pyruvate uptake which at 1 mM lactate was increased from 0.027 +/- 0.008(4) mumol/min per g liver at normal pH to 0.084 +/- 0.013(4) at low pH. At 10 mM lactate the liver produced pyruvate, but the production was significantly reduced by a lowering of the pH, being 0.45 +/- 0.13(8) mumol/min per g liver at pH 7.4 and 0.22 +/- 0.06(4) at pH 6.9. THe counterbalancing changes in lactate metabolism were too small to attain statistical significance. The stimulation of gluconeogenesis by an increase in FFA from 0 to 1 mM in the medium was unaffected by pH. Alanine uptake was decreased from 0.48 +/- 0.05(6) to 0.39 +/- 0.07(3) by lowering the pH from 7.4 to 6.9. We conclude that metabolic acidosis does not in itself inhibit the capacity of the perfused rat liver to remove lactate and pyruvate from the blood. If the same is true in man, no beneficial effect of bicarbonate treatment on lactate clearance in patients with lactic acidosis should be expected.