Effects of the dimethyl ester on succinic acid on the hormonal and metabolic response to exercise in hereditarily diabetic starved rats

This study was designed to assess the effect of the dimethyl ester of succinic acid (SAD) upon the hormonal and metabolic response to a 60-min exercise in overnight-starved Goto-Kakizaki rats. Twenty Goto-Kakizaki rats were starved overnight and then either maintained at rest or obliged to swim for 60 min. Half of the rats were injected intraperitoneally with the dimethyl ester of succinic acid (SAD, 5.0 micromol g(-1) body wt) immediately before exercise (or 60 min of rest). In the hereditarily diabetic rats, overnight starvation lowered the plasma D- glucose, insulin and lactate concentrations, while increasing that of free fatty acids and beta-hydroxybutyrate. In resting rats, the injection of SAD increased the glycogen content of liver, heart and muscle and the plasma concentration of D-glucose, insulin, glycerol and free fatty acids. In control animals, not injected with SAD, exercise increased the plasma concentration of D- glucose, lactate and glycerol, whilst lowering both that of insulin and the glycogen content of liver, heart and muscle. The injection of SAD before exercise failed to prevent and, on occasion, even accentuated the changes in both the glycogen content of liver, heart and muscle and the plasma concentration of D-glucose, insulin, glycerol and free fatty acids, whilst minimizing the increase in lactate concentration otherwise caused by exercise. Nevertheless, the comparison between resting and exercising rats, both injected with SAD, suggested that the ester abolished the exercise-induced rise in D-glucose, glycerol and fatty acid concentrations. By comparison with comparable experiments conducted in overnight-starved normal rats, these findings emphasize both the difference between normal and diabetic rats in their metabolic response to exercise, especially in terms of changes in glycemia, and the usefulness of SAD to compensate for the increased consumption of endogenous nutrients during exercise.     

The role of insulin in the control of triacyglycerol (TG) in the rat skeletal muscles

The role of insulin in the control of triacyglycerol (TG) in different types of skeletal muscle has not been fully recognized so the aim of the present study was to fill this gap. The experiments were carried out on control rats, those fed with olive oil or fed with the oil and treated with insulin and on streptozotocin diabetic animals at rest and there after exercise till exhaustion. The level of TG was measured in the white and red layers of the vastus lateralis, the soleus and the diaphragm. It was found that acute feeding with olive oil had no effect on TG level in either muscle type examined. Insulin administered to rats fed with oil increased TG level in the red vastus. Streptozotocin diabetes caused an increase in TG level in muscles with high oxidative potential. Exercise lowered the level of TG only in the red vastus of the diabetic rats. It is concluded that insulin may increase muscle TG level. Accumulation of TG in muscles of rats with acute diabetes is likely to be a result of the high plasma free fatty acid concentration. Acute insulin deficiency did not affect the muscle TG response to exercise.     

Regulation of glycogen metabolism in rat respiratory muscles during exercise

The effect of prolonged exercise on the glycogen level in the respiratory muscles (diaphragm--D, external intercostal--IE and internal--II) has been studied in four groups of rats: 1-control, 2-fasted for 24 h, 3-treated with nicotinic acid and 4-treated with propranolol. There was a sharp reduction in glycogen level in each muscle after 30 min exercise in the control and fasted groups. Exercise till exhaustion further lowered the glycogen level in D in the control group and in IE and II in the fasted group. In the fasted group, the level of glycogen in each muscle, at rest, and after 30 min exercise, and in IE and II muscles after exercise till exhaustion was lower than in the control group. Nicotinic acid did not affect the glycogen level either at rest or during exercise as compared with the control group. Propranolol increased the glycogen level in the muscles at rest and during 30 min exercise. It partially prevented glycogen mobilization in D and IE and fully in II during exercise till exhaustion. In the control group, 24 and 48 h after exercise till exhaustion, the level of glycogen in each muscle exceeded the resting control value. It is concluded that exercise-induced glycogen metabolism in the respiratory muscles differs in some respects from that in the limb or heart muscles.     

Effect of the exercise-induced increase in glucocorticoids on endurance in the rat

To investigate the effect of the increase in glucocorticoids during exercise on endurance, rats were either sham operated (SO) or adrenalectomized. All adrenalectomized rats were given a subcutaneously implanted corticosterone pellet at the time of adrenalectomy. Adrenalectomized rats were injected with corticosterone (ADX Cort) or corn oil (ADX) 5 min before exercise. Rats were killed at rest or after running on a treadmill (21 m/min, 15% grade) until exhaustion. SO rats ran 138 +/- 6 min compared with 114 +/- 9 min for ADX Cort and 89 +/- 8 min for ADX. All differences in run times were significant (P less than 0.05). Corticosterone levels were similar in exhausted SO and ADX Cort groups. ADX exhausted rats had corticosterone levels similar to resting values in SO and ADX rats. Inhibition of the rise in glucocorticoids during exercise had no effect on liver glycogen, liver adenosine 3',5'-cyclic monophosphate, plasma insulin, blood glucose, lactate, glycerol, or 3-hydroxybutyrate, plasma norepinephrine, or red quadriceps and soleus glycogen. Plasma free fatty acids were significantly depressed at exhaustion in ADX rats compared with SO. These data show that glucocorticoids exert effects within the time frame of a prolonged exercise bout and play a role in increasing endurance.     

Inhibition of adipose tissue lipolysis increases intramuscular lipid and glycogen use in vivo in humans

This study investigates the consequences of inhibition of adipose tissue lipolysis on skeletal muscle substrate use. Ten subjects were studied at rest and during exercise and subsequent recovery under normal, fasting conditions (control trial, CON) and following administration of a nicotinic acid analog (low plasma free fatty acid trial, LFA). Continuous [U-13C]palmitate and [6,6-2H2]glucose infusions were applied to quantify plasma free fatty acid (FFA) and glucose oxidation rates and to estimate intramuscular triacylglycerol (IMTG) and glycogen use. Muscle biopsies were collected to measure 1) fiber type-specific IMTG content; 2) allosteric regulators of hormone-sensitive lipase (HSL), glycogen phosphorylase, and pyruvate dehydrogenase; and 3) the phosphorylation status of HSL at Ser563 and Ser565. Administration of a nicotinic acid analog (acipimox) substantially reduced plasma FFA rate of appearance and subsequent plasma FFA concentrations (P < 0.0001). At rest, this substantially reduced plasma FFA oxidation rates, which was compensated by an increase in the estimated IMTG use (P < 0.05). During exercise, the progressive increase in FFA rate of appearance, uptake, and oxidation was prevented in the LFA trial and matched by greater IMTG and glycogen use. Differential phosphorylation of HSL or relief of its allosteric inhibition by long-chain fatty acyl-CoA could not explain the increase in muscle TG use, but there was evidence to support the contention that regulation may reside at the level of the glucose-fatty acid cycle. This study confirms the hypothesis that plasma FFA availability regulates both intramuscular lipid and glycogen use in vivo in humans.     

Influence of fasting on glycogen depletion in rats during exercise

We recently observed that a 24-h fasted group of rats could run longer than an ad libitum fed control group before becoming exhausted. Because of the demonstrated importance of glycogen levels and free fatty acid availability during endurance exercise, we have investigated several parameters of carbohydrate and lipid metabolism in exercised and nonexercised rats that were either fed ad libitum or fasted for 24 h. A 24-h fast depleted liver glycogen, lowered plasma glucose concentration, decreased muscle glycogen levels, and increased free fatty acid and beta-hydroxybutyrate concentrations in plasma. During exercise the fasted group had lower plasma glucose concentration, higher plasma concentration of free fatty acids and beta-hydroxybutyrate, and a lower muscle glycogen depletion rate than did the ad libitum fed group. Since fasted rats were able to continue running even when plasma glucose had dropped to levels lower than those of fed-exhausted rats, it seems unlikely that blood glucose level, per se, is a factor in causing exhaustion. These results suggest that fasting increases fatty acid utilization during exercise and the resulting "glycogen sparing" effect may result in increased endurance.     

Angiotensin II type 1 receptor blocker ameliorates overproduction and accumulation of triglyceride in the liver of Zucker fatty rats

The effects of angiotensin II type 1 receptor blocker (ARB) on triglyceride (TG) metabolism associated with insulin resistance were explored in Zucker fatty (ZF) rats. Olmesartan medoxomil, a newly developed ARB, was given as a 0.01% drinking solution ad libitum to ZF and Zucker lean (ZL) rats for 4 wk. Olmesartan lowered blood pressure in both strains to the same extent. ZF rats had a markedly low insulin sensitivity index (SI) and glucose effectiveness (SG), together with significantly increased glucose levels. Olmesartan treatment substantially elevated both SI and SG. The ZF rats were hyperlipidemic, with plasma TG levels sixfold higher than those of the ZL rats. Olmesartan remarkably decreased the plasma free fatty acid level in the ZF rats, but it did not exert a significant effect on the plasma TG level. The TG secretion rate assessed by the Triton WR-1339 technique was almost six times higher in the ZF than in the ZL rats, and olmesartan treatment suppressed this TG overproduction by one-half. The TG content in the liver was ten times higher in the ZF than in the ZL rats, and olmesartan halved this high hepatic TG content without affecting the cholesterol content. The fatty liver developed in the ZF rats was ameliorated by olmesartan treatment. Olmesartan treatment had no significant effects on TG metabolism or insulin sensitivity in the ZL rats. Taken in sum, ARB improves the overproduction and accumulation of TG in the liver associated with insulin resistance, and it does so through mechanisms independent of its hypotensive action.     

Conjugated docosahexaenoic acid inhibits lipid accumulation in rats

Conjugated linoleic acid (CLA), which contains a conjugated double-bond system, and n-3 highly unsaturated fatty acids such as docosahexaenoic acid (DHA) are widely known to improve lipid metabolism. To examine the possibility that a fatty acid with a combination of these structural features might have stronger physiological effects, we prepared conjugated DHA (CDHA) by alkaline isomerization of DHA and examined its effects on lipid and sugar metabolism in rats. Rats were force fed with 200 mg of test oils [linoleic acid (LA), DHA, CLA or CDHA] everyday for 4 weeks. Compared with the animals from the other groups, those in the CDHA group showed a significant weight loss in white adipose tissue (57% of adipose tissue weight in the LA group) and significant decreases in the levels of liver triacylglycerol (TG; 65% of TG level in the LA group) as well as total cholesterol (TC; 88% of TC level in the LA group), indicating suppression of lipid accumulation in the liver and adipose tissue. In addition, plasma TG and TC levels significantly decreased (69% of TG level and 82% of TC level in the LA group), indicating improved lipid metabolism. In the liver, the fatty acid synthesis system was inhibited and the fatty acid beta-oxidation system was activated, whereas the free fatty acid, glucose and tumor necrosis factor alpha levels in the plasma were lowered following CDHA administration. Hence, intake of CDHA appears to suppress the accumulation of fat in the liver and epididymal adipose tissue and improves lipid and sugar metabolism in rats.     

Modulation of insulin resistance and hypertension by voluntary exercise training in the TG(mREN2)27 rat.

Hypertension is often accompanied by insulin resistance of skeletal muscle glucose transport. The male heterozygous TG(mREN2)27 rat, which harbors a mouse transgene for renin, displays local elevations in the renin-angiotensin system and exhibits markedly elevated systolic blood pressure (SBP). The present study was undertaken to characterize insulin-stimulated skeletal muscle glucose transport in male heterozygous TG(mREN2)27 rats and to evaluate the effect of voluntary exercise training on SBP and skeletal muscle glucose transport. Compared with normotensive Sprague-Dawley rats, TG(mREN2)27 rats displayed a 53% elevation (P < 0.05) in SBP, a twofold increase in plasma free fatty acid levels, and an exaggerated insulin response during an oral glucose tolerance test. Moreover, insulin-mediated glucose transport (2-deoxyglucose uptake) in isolated epitrochlearis and soleus muscles of TG(mREN2)27 animals was 33 and 43% less, respectively, than in Sprague-Dawley controls. TG(mREN2)27 rats ran voluntarily for 6 wk and achieved daily running distances of 6-7 km over the final 3 wk. Training caused a 36% increase in peak aerobic capacity and a 16% reduction in resting SBP. Fasting plasma insulin (21%) and free fatty acid (34%) levels were reduced in the trained TG(mREN2)27 rats. Whole body glucose tolerance was improved in the trained TG(mREN2)27 rats and was associated with increases of 39 and 50% in insulin-mediated glucose transport in epitrochlearis and soleus muscles, respectively. Whole muscle GLUT-4 protein was increased in the soleus (23%), but not in the epitrochlearis, of trained TG(mREN2)27 rats. These data indicate that the male heterozygous TG(mREN2)27 rat is a model of both hypertension and insulin resistance. Importantly, both of these defects can be beneficially modified by voluntary exercise training.     

Effect of exercise on energy substrates metabolism in tissues of adrenalectomized rats

Effect of adrenalectomy and exercise on skeletal muscle, heart and liver glycogen and triglycerides, blood glucose and plasma free fatty acid level has been studied in the rat. It has been found that exercise-induced mobilization of glycogen in vastus deepest and soleus was diminished whereas utilization of liver glycogen was accelerated in adrenalectomized rats as compared to sham-operated controls. Triglyceride content in vastus deepest was reduced and in the liver increased in control rats but remained stable during exercise in adrenalectomized rats. In the latter group hypoglycemia occurred earlier and was more pronounced, whereas plasma free fatty acid level was markedly lower than in the control group.     

Effects of training on glucose metabolism of gluconeogenesis-inhibited short-term-fasted rats

To evaluate the effects of endurance training on gluconeogenesis and blood glucose homeostasis, trained as well as untrained short-term-fasted rats were injected with mercaptopicolinic acid (MPA), a gluconeogenic inhibitor, or the injection vehicle. Glucose kinetics were assessed by primed-continuous venous infusion of [U-14C]- and [6-3H]glucose at rest and during submaximal exercise at 13.4 m/min on level grade. Arterial blood was sampled for the determination of blood glucose and lactate concentrations and specific activities. In resting untrained sham-injected rats, blood glucose and lactate were 7.6 +/- 0.2 and 1.3 +/- 0.1 mM, respectively; glucose rate of appearance (Ra) was 71.1 +/- 12.1 mumol.kg-1.min-1. MPA treatment lowered blood glucose, raised lactate, and decreased glucose Ra. Trained animals had significantly higher glucose Ra at rest and during exercise. At rest, trained MPA-treated rats had lower blood glucose, higher blood lactate, and similar glucose Ra and disappearance rates (Rd) than trained sham-injected animals. Exercising sham-injected untrained animals had increased blood glucose and glucose Ra compared with rest. Exercising trained sham-injected rats had increased blood glucose and glucose Ra and Rd but no change in blood lactate compared with untrained sham-injected animals. In the trained animals during exercise, MPA treatment increased blood lactate and decreased blood glucose and glucose Ra and Rd. There was no measurable glucose recycling in trained or untrained MPA-treated animals either at rest or during submaximal exercise. There was no difference in running time to exhaustion between trained and untrained MPA-treated rats.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of glucose infusion on muscle malonyl-CoA during exercise

Previous work in this laboratory has shown that muscle malonyl-CoA, the inhibitor of carnitine palmitoyltransferase I (CPT I), decreased during exercise. Hepatic malonyl-CoA content decreases when glucose availability decreases such as during fasting or when the glucagon-to-insulin ratio increases such as during prolonged exercise or in response to insulin deficiency. To investigate the effect of glucose infusion on muscle malonyl-CoA during exercise, male rats were anesthetized (pentobarbital via venous catheters) at rest or after running (21 m/min, 15% grade) for 30 or 60 min. During exercise rats were infused with either glucose (0.625 g/ml) or saline at a rate of 1.5 ml/h. Gastrocnemius muscles and liver samples were frozen at liquid nitrogen temperature. Muscle malonyl-CoA decreased from 1.24 +/- 0.06 to 0.69 +/- 0.05 nmol/g with glucose infusion and to 0.43 +/- 0.04 nmol/g with saline infusion during 60 min of exercise. In the liver, glucose infusion prevented the drop in malonyl-CoA. This indicates that glucose infusion attenuates the progressive decline in muscle malonyl-CoA and prevents the decline in liver malonyl-CoA during prolonged exercise.     

6-OHDA sympathectomy and exercise performance in the rat.

6-hydroxydopamine (6-OHDA) was utilised for the study of the sympathetic nervous system in the resting rats and rats submitted to prolonged exercise. In order to reduce the acute physiological stress associated with an injection of 6-OHDA, beta-1 and alpha-1 adrenoceptors were blocked before the treatment leading to sympathectomy. Sympathectomised rats were divided in two groups: one sacrificed at rest, 24 hours after the treatment. The other group was sacrificed after a treadmill exercise to exhaustion. Running time to exhaustion was 36.0 +/- 4.5 min (mean +/- S.E.M.). This group ran significantly less than a control group brought to exhaustion in 73.7 +/- 10.0 min of exercise (P < 0.05). In order to make appropriate comparisons, another control group was run for 36 min. Some differences were observed between corresponding control and sympathectomized groups. At rest: 1) a lower plasma level of insulin, and 2) a higher plasma free fatty acid concentration were observed in sympathectomized rats. After 36 min of exercise: 1) a lower plasma concentration of norepinephrine, 2) no decrease of the plasma level of insulin, 3) no increase in the plasma glucagon concentration, and 4) a higher plasma glucose level were observed in sympathectomised rats when compared to control rats running for the same time. The lower plasma norepinephrine concentration in exercised sympathectomised rats suggests a lower sympathetic nervous activity in these animals than in control rats. The absence of a decrease of plasma insulin concentration and of an increase in glucagon can be attributed to this lower sympathetic activity in sympathectomised rats.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of hepatic vagotomy on postexercise substrate levels in food-restricted rats

The metabolic effects of a selective hepatic vagotomy (HV) were investigated at rest and immediately after a 50-min exercise period (26 m/min, 0% grade) in rats subjected to an overnight 50% food restriction. This dietary restriction reduced liver glycogen content to 50% of normal resting concentrations (2.2-2.8 g/100 g). No significant differences between HV and sham-operated rats were found in resting and exercising beta-hydroxybutyrate, glucose, glycerol, and insulin concentrations. Postexercise liver glycogen concentrations were reduced to approximately 1.0 g/100 g in both HV and sham-operated groups. This decrease was associated with significantly (P less than 0.01) lower postexercise glycogen levels in the soleus muscle of HV rats (2.6 times) along with higher plasma free fatty acid concentrations (P less than 0.01). These data provide evidence that HV combined with a progressive decrease in liver glycogen content may influence substrate regulation during exercise. They also support the concept of the existence of hepatic glucoreceptors responsive to a decrease in liver glycogen content.     

Muscle malonyl-CoA decreases during exercise

Malonyl-CoA, the inhibitor of carnitine acyltransferase I, is an important regulator of fatty acid oxidation and ketogenesis in the liver. Muscle carnitine acyltransferase I has previously been reported to be more sensitive to malonyl-CoA inhibition than is liver carnitine acyltransferase I. Fluctuations in malonyl-CoA concentration may therefore be important in regulating the rate of fatty acid oxidation in muscle during exercise. Male rats were anesthetized (pentobarbital via venous catheters) at rest or after 30 min of treadmill exercise (21 m/min, 15% grade). The gastrocnemius/plantaris muscles were frozen at liquid N2 temperature. Muscle malonyl-CoA decreased from 1.66 +/- 0.17 to 0.60 +/- 0.05 nmol/g during the exercise. This change was accompanied by a 31% increase in cAMP in the muscle. The decline in malonyl-CoA occurred before muscle glycogen depletion and before onset of hypoglycemia. Plasma catecholamines, corticosterone, and free fatty acids were all significantly increased during the exercise. This exercise-induced decrease in malonyl-CoA may be important for allowing the increase in muscle fatty acid oxidation during exercise.     

Metabolic and endocrine responses to prolonged exercise in rats under beta 2-adrenergic blockade

The respective roles of allosteric regulators and catecholamines in the control of muscle glycogen breakdown during exercise remain a matter of controversy. This study was designed to reassess the role of the sympathoadrenal system during prolonged exercise in rats. Animals were studied at rest or after treadmill exercise (28 m.min-1; 8% slope) to exhaustion in a control situation or following administration of a specific beta 2-adrenergic receptor antagonist (ICI 118,551, 1 mg.kg-1, i.v.). Running times to exhaustion were 54 and 36 min in control and treated rats, respectively. For the purpose of comparison, another group of control rats was studied after a 36-min exercise bout. The reduction in endurance in treated rats was associated with an impairment in glycogen utilization, as measured by muscle glycogen stores, in soleus muscle but not in superficial vastus lateralis or gastrocnemius lateralis muscles. Utilization of liver glycogen stores was similar in the two groups of animals, but plasma glucose (7 vs. 13 mM) and lactate (4 vs. 7 mM) levels were significantly lower in rats under beta-blockade than in control rats run for 36 min. Plasma free fatty acid and glycerol concentrations were not significantly different between groups. On the other hand, plasma epinephrine concentration was significantly higher in treated rats (13 vs. 5 mM), which might reflect a compensatory increase in adrenal activity. These results suggest that glycogen breakdown during prolonged exercise is under the control of the sympathoadrenal system in predominantly slow-twitch but not in predominantly fast-twitch muscles.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of selective hepatic vagotomy on running endurance in rats

The liver, through the afferent ways of the vagus hepatic nerve, may influence metabolic adaptations during exercise. This study assesses the functional significance of this hepatic innervation by determining the effect of a selective hepatic vagotomy (HV) on running endurance time during submaximal activity in rats subjected to an overnight 50% food restriction. The time to exhaustion was similar for the groups of HV and sham-operated (SHM) rats [66 +/- 15 vs. 64 +/- 21 (SD) min]. The HV group was associated with higher resting levels (P less than 0.05) of hepatic glycogen and plasma glucose. No significant differences were observed between HV and SHM rats at rest and after exercise for muscle glycogen, free fatty acids, insulin, glucagon, and lactate concentrations. These data indicate that if hepatic glucoreceptors do exist and contribute to the metabolic regulation of exercise, their functional significance is secondary to more important regulatory mechanisms.     

Reduction of Fructose-induced Hypertriglyceridemia and Fatty Liver in Rats by 4-(4′-Chlorobenzyloxy)benzyl Nicotinate (KCD-232)

The effect of KCD-232, a new compound with a structure of 4-(4′-chlorobenzyloxy)benzyl nicotinate, on fructose-induced hypertriglyceridemia and fatty liver was studied in rats refed experimental diets for 3 days after having been starved for 2 days.

In younger or older rats refed 7% corn oil-containing diets, both the serum and liver triglyceride (TG) levels were higher in the fructose (F) group than in the glucose (G) group, and those of the F group were higher in the older rats than the younger rats. KCD-232 effectively inhibited fructose-induced hypertriglyceridemia and fatty liver in both the younger and older rats. In older rats refed 7% corn oil diets, an increase in hepatic fatty acid (FA) synthesis and decreases in the activities of hepatic TG lipase (HTGL) and adipose tissue lipoprotein lipase (LPL) were found in the F group, while the serum free FA level and hepatic FA oxidative activity of the F group were equal to those of the G group. KCD-232 strongly inhibited the fructose-enhanced FA synthesis, slightly repressed the fructose-suppressed HTGL activity and had no effect on LPL activity and FA oxidation.

These results suggest that fructose-induced hypertriglyceridemia and fatty liver are due to an enhanced hepatic FA synthesis and decreased hydrolytic activities required for TG clearance from the circulation system and that KCD-232 prevents them by inhibiting enhanced FA synthesis.     

The protective effect of shrimp cooked in different methods on high-cholesterol- induced fatty liver in rats

This study examined the impact of different cooking methods on fatty acid (FAs) composition of shrimp meat and the ability of these foods to protect against high cholesterol (HC) diet-induced non-alcoholic fatty liver disease (NAFLD) in rats. Shrimp were cooked for 10 min boiled, grilled, or fried in sunflower oil. Rats (n = 6/group) were fed a normal diet (ND)or high-cholesterol diet (HC) each containing boiled, grilled or fried shrimp powder (15% w/w) (NDBS, NDFS, NDGS for ND or HCBS, HCFS, HCDGS for HC diet). Frying alone significantly reduced total levels of saturated FAs (SFA) and increased total mono- and polyunsaturated FAs (MSFA, and PUFAs, respectively) in shrimp meat. It also increased levels of n-6 PUFAs and linoleic acid (LA) and decreased levels of n-3 PUFAs including eicosapentaenoic FAs (EPA) and docosahexaenoic fatty acid (DHA). When fed to HC rats, only diets containing the grilled and boiled shrimp powders significantly prevented the weight loss, lowered fasting and glucose levels, improved glucose and insulin tolerance, and prevented the increase in serum liver markers, ALT and AST. They also reduced hepatic fat accumulation, reduced serum levels and hepatic levels of cholesterol and triglycerides (TGs), reduced hepatic levels of MDA, tumor necrosis factor-alpha (TNF-α), and IL-6, and increased those of glutathione (GSH) and superoxide dismutase (SOD). No alterations in all these parameters were observed in HC-fed rats which fed fried shrimp. In conclusion, boiling and grilling but not frying are the best method to cook shrimp to preserve their fatty acid content and its nutritional value in ameliorating NAFLD.     

Evidence that the decrease in liver glycogen is associated with the exercise-induced increase in IGFBP-1.

The purpose of the present study was to test the hypothesis that the exercise-induced increase in insulin-like growth factor binding protein (IGFBP)-1 is not always linked to a decrease in blood glucose level and to examine whether the decreasing levels of liver glycogen during exercise may be associated with the increase in IGFBP-1. Three groups of rats were submitted to a 70-min treadmill exercise. One group of rats was fed normally, and the two other groups had their food intake restricted by 50% (50% fast) the night before the experiment. One of these two 50% fasted groups of rats was infused (intravenously) with glucose throughout exercise to maintain euglycemia. Exercise in noninfused 50% fasted rats, compared with the normally fed rats, resulted in significantly lower blood glucose (minute 70) and insulin levels, significantly lower liver glycogen content, no change in IGF-I, and significantly higher increases in free fatty acid, glycerol, beta-hydroxybutyrate, and IGFBP-1. Maintenance of euglycemia during exercise in glucose-infused 50% fasted rats reduced to a large extent the decrease in insulin levels but only slightly attenuated the lipid response and the IGFBP-1 response seen in noninfused 50% fasted rats. Comparisons of all individual liver glycogen and IGFBP-1 values revealed that liver glycogen values were highly (P < 0.001) predictive of the IGFBP-1 response during exercise (R = 0.564). The present results indicate that the IGFBP-1 response during exercise is not always linked to a decrease in plasma glucose and suggest that the increase in IGFBP-1 during exercise may be related to the decrease in liver glycogen content.