Effect of endurance training on hypothalamic serotonin concentration and performance.

1. Serotonin is a neurotransmitter that modulates several functions, such as food intake, energy expenditure, motor activity, mood and sleep. Acute exhaustive endurance exercise increases the synthesis, concentration and metabolism of serotonin in the brain. This phenomenon could be responsible for central fatigue after prolonged and exhaustive exercise. However, the effect of chronic exhaustive training on serotonin is not known. The present study was conducted to examine the effect of exhaustive endurance training on performance and serotonin concentrations in the hypothalamus of trained rats. 2. Rats were divided into three groups: sedentary rats (SED), moderately trained rats (MOD) and exhaustively trained rats (EXT), with an increase of 200% in the load carried during the final week of training. 3. Hypothalamic serotonin concentrations were similar between the SED and MOD groups, but were higher in the EXT group (P < 0.05). Performance was lower in the EXT group compared with the MOD group (P < 0.05). 4. Thus, the present study demonstrates that exhaustive training increases serotonin concentrations in the hypothalamus, together with decreased endurance performance after inadequate recovery time. However, the mechanism underlying these changes remains unknown.

Creatine supplementation reduces plasma levels of pro-inflammatory cytokines and PGE2 after a half-ironman competition.

OBJECTIVE: The effect of creatine supplementation upon plasma levels of pro-inflammatory cytokines: Interleukin (IL) 1 beta and IL-6, Tumor Necrosis Factor alpha (TNFalpha), and Interferon alpha (INF alpha) and Prostaglandin E(2) (PGE(2)) after a half-ironman competition were investigated. METHODS: Eleven triathletes, each with at least three years experience of participation in this sport were randomly divided between the control and experimental groups. During 5 days prior to competition, the control group (n = 6) was supplemented with carbohydrate (20 g x d(-1)) whereas the experimental group (n = 5) received creatine (20 g x d(-1)) in a double-blind trial. Blood samples were collected 48 h before and 24 and 48 h after competition and were used for the measurement of cytokines and PGE(2). RESULTS: Forty-eight hours prior to competition there was no difference between groups in the plasma concentrations (pg x ml(-1), mean +/- SEM) of IL-6 (7.08 +/- 0.63), TNFalpha (76.50 +/- 5.60), INF alpha (18.32 +/- 1.20), IL-1 beta (23.42 +/- 5.52), and PGE(2) (39.71 +/- 3.8). Twenty-four and 48 h after competition plasma levels of TNFalpha, INF alpha, IL-1 beta and PGE(2) were significantly increased (P < 0.05) in both groups. However, the increases in these were markedly reduced following creatine supplementation. An increase in plasma IL-6 was observed only after 24 h and, in this case, there was no difference between the two groups. CONCLUSION: Creatine supplementation before a long distance triathlon competition may reduce the inflammatory response induced by this form of strenuous of exercise.

Endurance training restores peritoneal macrophage function in post-MI congestive heart failure rats.

Congestive heart failure (CHF) induces a state of immune activation, and peritoneal macrophages (M phi s) may play an important role in the development and progression of one such condition. Moderate endurance training modulates peritoneal M phi function. We evaluated the effect of endurance training on different stages of the phagocytic process and in the production of interleukin-6 (IL-6), interleukin-1beta (IL-1beta) and tumor necrosis factor-alpha (TNF-alpha) after LPS stimulation. Either ligation of the left coronary artery or Sham operations were performed in adult Wistar rats. After 4 wk, control (Sham operated) and MI (ligation of the left coronary artery) animals were randomly assigned to either a sedentary (Sham-operated sedentary, n = 7 and MI sedentary, n = 10) or a trained group (Sham-operated trained, n = 8 and MI trained, n = 8). Trained rats ran on a treadmill (0% grade at 13-20 m/min) for 60 min/day, 5 days/wk, for 8-10 wk, whereas sedentary rats had only limited activity. Training increased maximal oxygen uptake normalized for body weight (ml.kg(-1).min(-1)), as well as skeletal muscle citrate synthase maximal activity, when compared with sedentary groups. The resident and total cell number, the chemotaxis index, and the production of TNF-alpha stimulated by LPS were significantly higher in the MI sedentary group when compared with the Sham sedentary group. Moderate endurance training reversed these alterations promoted by post-MI. These results demonstrate that moderate intensity exercise training modulates peritoneal M phi function and induces beneficial metabolic effects in rats with post-MI CHF.

Effects of a 30-km race upon salivary lactate correlation with blood lactate.

Blood lactate has been used to determine the aerobic capacity and long distance performance. Recently, a new methodology has been suggested to supplant the invasive blood lactate techniques. Salivary lactate has received attention because it shows high correlation to blood lactate in progressive overload test. We evaluated the correlation between salivary and blood lactate during a long distance run and assessed possible changes in salivary lactate concentration. Fifteen expert marathon racers ran 30 km as fast as possible. Saliva and 25 muL of blood were collected at rest and at each 6 km for lactate determination. Blood lactate concentration increased in the 6th km and then remained constant until the end of the race. Salivary lactate increased after 18 km in relation to basal. We found high correlations between blood and saliva absolute lactate (r=0.772, p<0.05) and the blood lactate relative concentration corrected by protein (r=0.718, p<0.05). The highest correlation found between absolute and relative salivary lactate was r=0.994 (p<0.001). Our results show that it is possible to use salivary lactate with absolute values or relative protein concentration. In addition, salivary lactate showed a high correlation with blood lactate in endurance events.

Plasma glutamine concentration in spinal cord injured patients.

Glutamine, a non-essential amino acid, is the most important source of energy for macrophages and lymphocytes. Reduction in its plasma concentration is related with loss of immune function, as leukocyte proliferation and cytokine production. It is well known that glutamine is largely produced by the skeletal muscle which is severely compromised as a consequence of the paralysis due to the damage of the spinal cord. In spinal cord injury (SCI) patients, infections, such as pneumonia and sepsis in general, are a major cause of morbidity and mortality. In comparison with the control group, a 54% decrease in plasma glutamine concentration was observed as well as a decrease in the production of TNF and IL-1 by peripheral blood mononuclear cells cultivated for 48 h in SCI patients. Therefore, we propose that a decrease in plasma glutamine concentration is an important contributor to the immunosuppression seen in SCI patients.

Effect of thioglycollate and BCG stimuli on glucose and glutamine metabolism in rat macrophages.

The macrophage is a differentiated cell that takes part in a wide range of physiological and pathological processes, such as inflammatory and immunological responses. The stimulation of macrophages involves the acquisition of some functional characteristics such as phagocytosis, ability to kill tumor cells, and processing and presentation of antigens. In this study we have investigated the changes in macrophage glucose and glutamine metabolism as induced by stimulation by thioglycollate (inflammatory) and bacille Calmette-Guérin (BCG) (activated). The results showed an increase in hexokinase and citrate synthase activities, due to both stimulatory processes. One difference between inflammatory and activated cells is the higher rate of glucose oxidation in the latter. The activation with BCG, however, also led to an enhancement in glutamine metabolism that is not observed in the inflammatory cell. These results suggest that glutamine metabolism might be important for macrophage function during immunological response.

Tryptophan consumption and indoleamines production by peritoneal cavity macrophages.

Melatonin has been shown to regulate several immune functions, and some authors showed that leukocytes are also able to produce the indolamine. In fact, it seems to take part in some immunoregulatory axis, including that related to interferon (IFN) production. So, we evaluated the rate of tryptophan consumption and melatonin and serotonin production in peritoneal cavity-isolated macrophages and the effect of IFN-alpha and -gamma, lipopolysaccharide (LPS), and phorbol myristate acetate (PMA) on such parameters. Our results indicate that macrophages obtained from the peritoneal cavity of normal rats when incubated with tryptophan show an increase in arylalkylamine N-acetyltransferase activity that corresponds to an increased melatonin production, as determined in the incubation medium. This process is regulated by IFN-alpha and -gamma, PMA, LPS, and the serum from tumor-bearing rats, opening the possibility of speculation about different immunoregulatory loops acting through the balance of melatonin/serotonin production by such cells.

Human macrophage metabolism of low density lipoprotein oxidized by stimulated neutrophils and ferritin.

The metabolism of low density lipoprotein (LDL) oxidized with phorbol myristate acetate (PMA) stimulated neutrophils plus ferritin (LDLox) by human monocyte-derived macrophage (HMDM) was studied. Binding of 125I-labeled LDLox to HMDM and further uptake and degradation were higher than for native 125I-labeled LDL. LDLox seems to be taken up by HMDM through the scavenger receptor as indicated by competition studies with unlabeled native and autoxidized LDL. An increased concentration of cellular cholesteryl esters was observed in HMDM exposed to LDLox. Oxidative modification of LDL increased its electrophoretic migration on agarose gel and also the fragmentation of apolipoprotein B. Data suggest that LDLox is incorporated by human macrophages and can potentially induce foam-cell formation.

The effect of melatonin chronic treatment upon macrophage and lymphocyte metabolism and function in Walker-256 tumour-bearing rats.

Melatonin is the main hormone involved in the neuroendocrine-immune axis. It also presents antitumour activity. To evaluate the role of melatonin on the progression of Walker-256 tumour in rats we determined the effect of the hormone on some biochemical and functional aspects of macrophage and lymphocytes from cachectic rats. An important finding observed in immune cells from tumour-bearing (TB) rats is the impairment on glutamine and glucose metabolism in such cells. These changes are very similar to those observed in pinealectomized rats (PNX). The increased production of lactate and the flux of glucose through the Krebs cycle and the reduction in glutamine consumption seems to be involved in the immunosuppression presented in the TB and PNX animals. Melatonin treatment restored the changes observed in the metabolism of glucose and glutamine and stimulated the proliferation of lymphocytes from tumour-bearing rats. The results indicate that the effect of melatonin upon tumour growth involves the stimulation of the immune system by the hormone.

Effect of epinephrine on glucose metabolism and hydrogen peroxide content in incubated rat macrophages.

The effects of epinephrine on glucose metabolism and hydrogen peroxide content were examined in incubated rat macrophages. An increase in the activities of hexokinase and citrate synthase and a reduction in that of glucose-6-phosphate dehydrogenase was found in resident, inflammatory and activated macrophages incubated for 1 hr in the presence of epinephrine. Glucose utilization by incubated resident, inflammatory and activated macrophages was augmented markedly by the addition of epinephrine, whereas lactate formation was depressed. Under the same conditions, there was a 2.6-fold increment of hydrogen peroxide content and of [U-14C]glucose decarboxylation in activated macrophages incubated for 40 min. Similar results were obtained when pyruvate and oxoglutarate was substituted for glucose. These findings suggest that epinephrine may increase hydrogen peroxide production in activated macrophages possibly through a mitochondrial mechanism other than the pentose-phosphate pathway. Between 40 and 90 min of incubation, the content of hydrogen peroxide decreased markedly, and there was no detectable glucose utilization in the presence of epinephrine. These observations are consistent with the idea that this catecholamine stimulates both hydrogen peroxide production and metabolism, the first process being dependent on mitochondrial fuels.

Carbohydrate supplementation during intense exercise and the immune response of cyclists.

OBJECTIVE: To evaluate the effect of carbohydrate supplementation upon some aspects of the immune function in athletes during intense indoor cycling. METHODS: Twelve male athletes cycled for 20 min at a velocity corresponding to 90% of that obtained at the anaerobic threshold and rested for 20 min. This protocol was repeated six times. The athletes received, during the trial, water ad libitum, or a solution of carbohydrate (95% glucose polymers and 5% fructose) at 10% (w/v), 1 g kg h every 20 min, starting at the 10th minute of the first exercise period, plus extra water ad libitum. RESULTS: Exercise induced a reduction in peripheral blood mononuclear cell proliferation (37%) as well as in the production of cytokines by cultured cells (interleukin-1 (IL-1), interleukin-2 (IL-2), tumor necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma), by 37%, 35%, 26% and 16%, respectively). All of these changes were prevented by the ingestion of a carbohydrate drink by the athletes, except that in IFN-gamma production, which was equally decreased (17%) after the second trial. The concentration of plasma glutamine, an important fuel for immune cells, was decreased in the placebo group but maintained in the group that received carbohydrate. CONCLUSION: Carbohydrate supplementation affects positively the immune response of cyclists by avoiding or minimizing changes in plasma glutamine concentration.

Immunosuppression in undernourished rats: the effect of glutamine supplementation.

OBJECTIVE: The aim of our study is to determine the effect of a 30-day-period caloric restriction (CR) upon the immune response of rats and the influence of glutamine upon mononuclear cells proliferation and cytokine production. METHODS: Male albino Wistar rats were submitted to CR receiving an amount of food equivalent to 50% of the mean amount consumed by the control animals. We measured the incorporation of [2-14C]-thymidine by lymphocytes obtained from the spleen and mesenteric lymph nodes, plasma glucose and glutamine concentration, as well as cytokine production by cultivated cells, in the presence of glutamine. RESULTS: Rats submitted to CR presented reduced body weight (49%) and decreased splenic leukocyte number. CR led to a reduction in the proliferative response of lymphocyte. Spleenocytes from CR animals produced less gamma-interferon and interleukins 1, 4 and 10 in 48 h culture than did those from control rats. The same pattern is observed in cells obtained from the mesenteric lymph nodes. The addition of glutamine 2mM to the culture medium restored spleen and mesenteric lymph node cells' proliferative response and the production of interleukin 2 by cells obtained from the spleen and from the mesenteric lymph nodes. CONCLUSIONS: The present data reinforce that undernutrition decreases in vitro immune cell function and indicates that, in such circumstances, glutamine supplementation could reverse some of the changes observed in the functionality of cultured immune cells. The presence of the amino acid at physiological concentration, however, reinforces the diversion of the immune response towards a Th(1)-like response.

Effects of feeding lipids of different fatty acid compositions upon rat lymphocyte proliferation.

Weanling Wistar rats were fed for 8 weeks on a low fat (3% by weight) diet (LF) or on diets containing 15% by weight hydrogenated coconut oil (coconut oil), cocoa butter, cashew kernel oil (cashew oil), canola oil or soya bean oil (soya oil). Each of the high fat diets resulted in inhibition of spleen lymphocyte proliferation in response to concanavalin A (Con A), a T-cell mitogen. Feeding the soya oil diet caused more than 95% inhibition of proliferation, compared with feeding the LF diet. Amongst the high fat diets, feeding the cashew, canola or soya oil diets resulted in inhibition of proliferation compared with feeding the coconut oil diet while feeding the soya oil diet resulted in inhibition of proliferation compared with feeding the cocoa butter or canola oil diets. Proliferation of lymphocytes in response to Con A was also investigated using whole blood culture. Once again, feeding the soya oil diet resulted in a dramatic decrease in proliferation (80%) compared with feeding the LF diet. Feeding the soya oil diet also inhibited proliferation compared with feeding the coconut oil, cocoa butter or cashew oil diets. Feeding the canola oil diet resulted in inhibition of proliferation compared with feeding the LF or cocoa butter diets.

The effect of creatine supplementation upon inflammatory and muscle soreness markers after a 30km race.

We have evaluated the effect of a creatine supplementation protocol upon inflammatory and muscle soreness markers: creatine kinase (CK), lactate dehydrogenase (LDH), prostaglandin E2) (PGE2) and tumor necrosis factor-alpha (TNF-alpha) after running 30km. Runners with previously experience in running marathons, with their personal best between 2.5-3h were supplemented for 5 days prior to the 30km race with 4 doses of 5g of creatine and 15g of maltodextrine per day while the control group received the same amount of maltodextrine. Pre-race blood samples were collected immediately before running the 30km, and 24h after the end of the test (the post-race samples). After the test, athletes from the control group presented an increase in plasma CK (4.4-fold), LDH (43%), PGE2 6.6-fold) and TNF-alpha (2.34-fold) concentrations, indicating a high level of cell injury and inflammation. Creatine supplementation attenuated the changes observed for CK (by 19%), PGE2 and TNF-alpha (by 60.9% and 33.7%, respectively, p<0.05) and abolished the increase in LDH plasma concentration observed after running 30km, The athletes did not present any side effects such as cramping, dehydration or diarrhea, neither during the period of supplementation, nor during the 30km race. All the athletes finished the race in a time equivalent to their personal best +/- 5.8%. These results indicate that creatine supplementation reduced cell damage and inflammation after an exhaustive intense race.

Glutamine metabolism is changed in lymphocytes from aged rats.

Changes in the protein content, maximal activity, and Km of phosphate-dependent glutaminase were measured in the lymphoid organs (thymus, spleen, and mesenteric lymph nodes) from just-weaned, mature (3 months), and aged rats (15 months). Also, [U-14C] glutamine transport and decarboxylation and the production of glutamate and aspartate from 2 and 20 mM glutamine were measured in incubated mesenteric lymph node lymphocytes. The ageing process induced a reduction in the protein content of the thymus and spleen, as well as the phosphate-dependent glutaminase activity in the thymus and isolated lymphocytes. The Km of phosphate-dependent glutaminase, however, was not affected by the process. Ageing reduced [U-14C] glutamine decarboxylation and increased glutamate and aspartate production in incubated lymphocytes. The results indicate that the ageing process does modify several aspects of glutamine metabolism in lymphocytes: reduces maximal glutaminase activity and [U-14C] glutamine decarboxylation and increases the Km for [U-14C] glutamine uptake and the production of glutamate and aspartate.

Superoxide dismutase, catalase, and glutathione peroxidase activities in muscle and lymphoid organs of sedentary and exercise-trained rats.

The effect of swimming-training upon the activities of the enzymes involved in the generation of reducing-equivalents (citrate synthase-mitochondria and glucose-6-phosphate dehydrogenase-cytosol) and of antioxidant enzymes (CuZn- and Mn-SOD, catalase and glutathione peroxidase) in the lymphoid organs (thymus, mesenteric lymph nodes and spleen) was examined. The skeletal muscles (soleus-red and gastrocnemius-white) were also studied. Although our data suggest an apparently random, organ-specific change in enzymatic activity, some interesting trends can be observed. Firstly, the increased citrate synthase and Mn-SOD activities observed in red, but not in white muscle, corroborate the well-known effect of endurance exercise-training on mitochondrial oxidative metabolism. Secondly, there was an inverse relationship between TBARs-monitored lipoperoxidation and glutathione peroxidase activity in all tissues studied, what is in accordance with the previous findings showing that such enzyme exerts the fine control of intracellular lipoperoxide concentration. Except in the case of the spleen, there was a trend for elevated glucose-6-phosphate dehydrogenase activity, coadjuvant of glutathione peroxidase in the antioxidant response to physical exercise in all tissues. Thirdly, Mn-SOD and catalase were conspicuously associated to oxidative stress in the thymus, while glutathione and catalase could be linked to this parameter in the spleen. Fourthly, the lymph nodes seem to be more dependent on the glucose-6-phosphate dehydrogenase/glutathione peroxidase pair for protection against damage promoted by physical exercise. Mn-SOD and catalase activities were lower in the lymph nodes after swimming training.(ABSTRACT TRUNCATED AT 250 WORDS)

The effect of BCAA supplementation upon the immune response of triathletes.

INTRODUCTION: Intense long-duration exercise could lead to immune suppression through a decrease in the circulating level of plasma glutamine. The decrease in plasma glutamine concentration as a consequence of intense long-duration exercise was reversed, in some cases, by supplementing the diet of the athletes with branched-chain amino acids (BCAA). To better address this question, we have evaluated some blood parameters (lymphocyte proliferation, the level of plasma cytokines, plasma glutamine concentration, and in vitro production of cytokines by peripheral blood lymphocytes) before and after the São Paulo International Triathlon, as well as the incidence of symptoms of infections between the groups. METHODS: Twelve elite male triathletes of mean age 25.5 +/- 3.2 yr (ranging from 21.4 to 30.1 yr), weighing 74.16 +/- 3.9 kg, swam 1.5 km, cycled 40 km, and ran 10 km (Olympic triathlon) in the São Paulo International Triathlon held in April 1997 and April 1998. In both events, six athletes received BCAA and the others, placebo. RESULTS: Athletes from the BCAA group (BG) presented the same levels of plasma glutamine, before and after the trial, whereas those from the placebo group showed a reduction of 22.8% in plasma glutamine concentration after the competition. Changes in the proliferative response of peripheral blood lymphocytes were accompanied by a reduction in IL-1 production after exercise (22.2%), which was reversed by BCAA supplementation (20.3%), without changes in IL-2 production. DISCUSSION: The data obtained show that BCAA supplementation can reverse the reduction in serum glutamine concentration observed after prolonged intense exercise such as an Olympic triathlon. The decrease in plasma glutamine concentration is paralleled by an increased incidence of symptoms of infections that results in augmented proliferative response of lymphocytes cultivated in the absence of mitogens. The prevention of the lowering of plasma glutamine concentration allows an increased response of lymphocytes to ConA and LPS, as well as an increased production of IL-1 and 2, TNF-alpha, and IFN-gamma, possibly linked to the lower incidence of symptoms of infection (33.84%) reported by the supplemented athletes.

Fatty acid oxidation in lymphocytes from Walker 256 tumor-bearing rats.

The oxidation of fatty acids in lymphocytes from the mesenteric lymph nodes of Walker 256 carcinosarcoma-bearing rats (TB) was studied, as well as the activity of the mitochondrial long-chain fatty acid transport system. Two-month old Wistar rats were subcutaneously implanted with 10(7) cells and after 2 weeks the tumor mass was 15-20% of the carcass weight. The activity of carnitine palmitoyltransferase (CPT) II was demonstrable in the lymphocytes of the TB group (8.2 +/- 5.6 nmol/min per mg mitochondria protein for 15 rats) and was not detected in the control, while that of CPT I was only slightly increased in the former. Similar rates of [1-14C]-palmitate decarboxylation were found for TB and control rat lymphocytes. However, when the rate of decarboxylation of [1-14C]-palmitate present in the intracellular pool of lipids was investigated in cultured lymphocytes, the cells of TB rats exhibited rates 17-fold higher than those of control animals in the presence of fetal calf serum (FCS). Decarboxylation in the presence of TB rat serum was 178-fold higher than obtained with normal rat serum, and 1.4-fold compared to FCS. These results suggest that, during cachexia, lymphocytes preferably oxidize intracellular lipids, and that this capacity is greatly enhanced by factors circulating in the serum of tumor-bearing rats.

Changes in the TBARs content and superoxide dismutase, catalase and glutathione peroxidase activities in the lymphoid organs and skeletal muscles of adrenodemedullated rats.

Thiobarbituric acid reactant substances (TBARs) content, and the activities of glucose-6-phosphate dehydrogenase (G6PDh), citrate synthase (CS), Cu/Zn- and Mn-superoxide dismutase (SOD), catalase, and glutathione peroxidase (GPX) were measured in the lymphoid organs (thymus, spleen, and mesenteric lymph nodes (MLN)) and skeletal muscles (gastrocnemius and soleus) of adrenodemedullated (ADM) rats. The results were compared with those obtained for sham-operated rats. TBARs content was reduced by adrenodemedullation in the lymphoid organs (MLN) (28%), thymus (40%) and spleen (42%)) and gastrocnemius muscle (67%). G6PDh activity was enhanced in the MLN (69%) and reduced in the spleen (28%) and soleus muscle (75%). CS activity was reduced in all tissues (MLN (75%), spleen (71%), gastrocnemius (61%) and soleus (43%)), except in the thymus which displayed an increment of 56%. Cu/Zn-SOD activity was increased in the MLN (126%), thymus (223%), spleen (80%) and gastrocnemius muscle (360%) and was reduced in the soleus muscle (31%). Mn-SOD activity was decreased in the MLN (67%) and spleen (26%) and increased in the thymus (142%), whereas catalase activity was reduced in the MLN (76%), thymus (54%) and soleus muscle (47%). It is particularly noteworthy that in ADM rats the activity of glutathione peroxidase was not detectable by the method used. These data are consistent with the possibility that epinephrine might play a role in the oxidative stress of the lymphoid organs. Whether this fact represents an important mechanism for the establishment of impaired immune function during stress remains to be elucidated.

Effect of a polyunsaturated fatty acid-rich diet on macrophage and lymphocyte metabolism of diabetic rats.

Diabetic subjects present high susceptibility to infections but the mechanisms involved are not fully known. Macrophages and lymphocytes utilize glucose and glutamine at high rates and these metabolites are important for the function of these cells. The present study examines the activities of key metabolic enzymes in macrophages and lymphocytes obtained from alloxan-diabetic Wistar rats (10 weeks old, 7 rats each group). Since the enteral diet was enriched with omega-6 polyunsaturated fatty acids (PUFA), the effect of these fatty acids was also investigated in the same animals. Diabetes caused a marked decrease of hexokinase activity (48%; 274.23 +/- 18.43 vs 143.29 +/- 10.35 units for control vs diabetic rats) in macrophages and of citrate synthase and glucose-6-phosphate dehydrogenase activities (70%; 321.76 +/- 9.18 vs 96.25 +/- 5.43 units for citrate synthase and 89.43 +/- 2.33 vs 23.13 +/- 1.09 units for G6PDh for control vs diabetic rats) in mesenteric lymph node lymphocytes. A PUFA-rich diet given for 6 weeks enhanced hexokinase activities by 30% (274.23 +/- 18.43 vs 342.48 +/- 15.39, balanced vs PUFA-rich diets for normal and 143.29 +/- 10.35 vs 189.67 +/- 9.57 for diabetic rats) and reduced citrate synthase activities by 43% (30.31 +/- 1.73 vs 17.42 +/- 0.95, balanced vs PUFA-rich diets for normal and 29.34 +/- 1.23 vs 16.73 +/- 1.02 for diabetic rats) in macrophages, and reduced (< 50%; 59.67 +/- 3.45 vs 48.87 +/- 3.37 for hexokinase and 321.76 +/- 2.33 vs 161.66 +/- 9.97 for citrate synthase, balanced vs PUFA-rich diets) the activities of both enzymes in lymphocytes.(ABSTRACT TRUNCATED AT 250 WORDS)