Fat crystallisation at oil-water interfaces.

This review focuses on recent advances in the understanding of lipid crystallisation at or in the vicinity of an interface in emulsified systems and the consequences regarding stability, structure and thermal behaviour. Amphiphilic molecules such as emulsifiers are preferably adsorbed at the interface. Such molecules are known for their ability to interact with triglycerides under certain conditions. In the same manner that inorganic crystals grown on an organic matrix see their nucleation, morphology and structure controlled by the underlying matrix, recent studies report a templating effect linked to the presence of emulsifiers at the oil/water interface. Emulsifiers affect fat crystallisation and fat crystal behaviour in numerous ways, acting as impurities seeding nucleation and, in some cases, retarding or enhancing polymorphic transitions towards more stable forms. This understanding is of crucial importance for the design of stable structures within emulsions, regardless of whether the system is oil or water continuous. In this paper, crystallisation mechanisms are briefly described, as well as recent technical advances that allow the study of crystallisation and crystal forms. Indeed, the study of the interface and of its effect on lipid crystallisation in emulsions has been limited for a long time by the lack of in-situ investigative techniques. This review also highlights reported interfacial effects in food and pharmaceutical emulsion systems. These effects are strongly linked to the presence of emulsifiers at the interface and their effects on crystallisation kinetics, and crystal morphology and stability.

Triiodothyronine deiodinating activity in brown adipose tissue after short cold stimulation test in trained and untrained rats.

Interscapular brown adipose tissue (IBAT) activity is controlled by sympathetic nervous system, and factors that influence thermogenesis appear to be centrally connected to the sympathetic outflow to IBAT. Cold exposure produces a rise in BAT temperature, which is associated with an increased thyroid activity, elevated serum levels of 3,5,3'-triiodothyronine (T3), and an increased rate of T3 production. This study evaluated the effect of swimming training on 5'-triiodothyronine deiodinase (5'-D) activity in IBAT under normal environmental conditions and after short (30 min) cold exposure (TST stimulation test). 5'-D activity is lower in trained rats at basal condition, and TST increases 5'-D in IBAT of both untrained and trained rats. However, this increase is lower in trained rats. Training reduces the deiodinating activity in normal environmental conditions as well as after short cold exposure. Probably, other compensatory mechanisms of heat production are active in trained rodents.

Ibotenate lesion of the ventromedial hypothalamus lowers hyperthermic effects of prostaglandin E1.

This experiment tested the effects of an intracerebroventricular injection of prostaglandin E1 on the sympathetic activation and the thermogenic changes in rats with ibotenate lesions of the ventromedial hypothalamus. Under pentobarbital anesthesia, twelve Sprague-Dawley male rats were lesioned bilaterally in the ventromedial hypothalamus with an injection of ibotenic acid (30 nmol into each side). Sham lesions were carried out in other twelve control rats. After 48 h, all animals were anesthetized with ethyl-urethane. The firing rate of the sympathetic nerves innervating the interscapular brown adipose tissue and the colonic and interscapular brown adipose tissue temperatures were monitored before and after an intracerebroventricular injection of prostaglandin E1 (500 ng) or saline. Prostaglandin E1 induced an increase in the firing rate of sympathetic nerves and the colonic and interscapular brown adipose tissue temperatures. These effects were reduced by the ventromedial hypothalamic lesion. Since ibotenic acid destroys cell bodies, the findings indicate that neurons of the ventromedial hypothalamus play a considerable role in the control of sympathetic activation and the thermogenic changes during prostaglandin E1 hyperthermia.

The effects of prolonged peritendinous administration of PGE1 to the rat Achilles tendon: a possible animal model of chronic Achilles tendinopathy.

We studied the effects of peritendinous Achilles tendon injections of prostaglandin E1 (PGE1) on the Achilles tendon of rats. Five groups of Sprague-Dawley rats (n = 24 each) were studied. Groups 1 to 4 received weekly peritendinous injections. In group 1, one side was injected with 800 ng of PGE1 in 0.5 ml of 0.9% NaCl and the contralateral side was injected with 0.5 ml of 0.9% NaCl. In group 2, one side was injected with 800 ng of PGE1. In group 3, one side was injected with 0.5 ml of 0.9% NaCl. In group 4, a syringe needle was inserted in the peritenon unilaterally, but no substances were administered. In groups 2, 3, and 4, the contralateral tendon was used as the control. In group 5, treatment was not administered. Eight rats in each group were killed at each time point, after 7, 21, and 35 days of treatment. On day 7, values for average water content and average wet weight of the tendons treated with PGE1 were significantly higher than those in the control tendons (analysis of variance [ANOVA]; P = 0.02), with a histological picture of acute inflammation. On day 21, approximately half of the PGE1-treated tendons showed fibrosis of the paratenon, with adhesions and intra-tendinous degeneration, with the other half still showing a picture of acute inflammation. On day 35, all of the PGE1-treated tendons showed fibrosis of the paratenon, with adhesions and intra-tendinous degeneration. At all time points, there was no evidence of pathology in the tendons that had not received PGE1. Sham peritendinous injections and injections of normal saline did not produce inflammation in the Achilles tendons. Initially, local administration of PGE1 produced acute inflammation of the tendon and its surrounding tissues. Prolonged PGE1 administration produced peri- and intra-tendinous degeneration, providing a cheap, reproducible model of Achilles tendinopathy, which would allow studies of the effects of conservative and surgical management of the condition.

Cortical spreading depression reduces paraventricular activation induced by hippocampal neostigmine injection.

The firing rate of the neurons of the hypothalamic paraventricular nucleus, the temperatures of the interscapular brown adipose tissue and of the colon (TIBAT and Tc) were monitored in 24 urethane-anesthetized male Sprague-Dawley rats divided into four groups. These variables were measured before and after hippocampal injection of neostigmine (5x10(-7) mol) in the 1st and 2nd groups or of saline in the 3rd and 4th groups. The hippocampal injection was preceded by cortical spreading depression in the 1st and 3rd groups, while the cortical depression was not induced in the 2nd and 4th groups. The results show an increase of firing rate, TIBAT and Tc after neostigmine injection in the rats without cortical depression. Cortical spreading depression significantly reduces these enhancements. These findings demonstrate that: (1) the paraventricular nucleus plays a significant role in the hyperthermia induced by neostigmine injection into the hippocampus; and (2) the cerebral cortex is involved in the control of the paraventricular activity.

Eating Behavior is Associated to Sympathetic Activation Induced by ICV Injection of Prostaglandin E1 in the Rat.

This experiment tests the effect of intracerebro-ventricular (icv) injection of prostaglandin E1 (PGE1) on. (1) food intake, (2) sympathetic activity and body temperature. The firing rate of the sympathetic nerves to interscapular brown adipose tissue (IBAT), along with IBAT and colonic temperatures (TIBAT and TC) were monitored in male Sprague-Dawley rats before and for 90 min after food presentation. An icv injection of PGE1 (500 ng) or saline was made immediately before food presentation. The amount of food ingested was also measured. The same procedure was carried out in control rats without food presentation. The results show that PGE1 raises the sympathetic firing rate, TIBAT and TC and it causes a decrease in food intake. These findings suggest that the food intake is associated to the sympathetic activity in the PGE1-hyperthermia.

Sucrose rich diet modifies thermogenic response to injection of muscimol into the posterior hypothalamus in the rat.

The firing rate of the nerves innervating interscapular brown adipose tissue, temperatures of colon and interscapular brown adipose tissue, heart rate and oxygen consumption were monitored in urethane-anaesthetized male Sprague-Dawley rats fed with a sucrose rich diet. These variables were measured for 40 min before (baseline values) and 40 min after a 56 ng muscimol injection into the posterior hypothalamus. The same variables were monitored in other rats fed with a laboratory standard diet. Saline was injected into the posterior hypothalamus of control rats fed with sucrose or standard diet. Muscimol injection induced a decrease in firing rate, interscapular brown adipose tissue and colonic temperatures and oxygen consumption. This reduction was more evident in the rat fed with a sucrose rich diet than animals fed with standard diet. The kind of diet did not modify the decrease in heart rate induced by muscimol. These findings suggest that a sucrose rich diet modifies GABA-ergic responses to muscimol injection into the posterior hypothalamus.

Nitric oxide reduces hypophagia induced by threonine free diet in the rat.

Food intake and concentrations of glutamic (GLU) and aspartic (ASP) acids in the nucleus accumbens were monitored in male Sprague-Dawley rats fed a threonine free diet. These variables were measured before and after an intracerebroventricular injection of 20 nmole nitroprusside (NP), a non-enzymatic nitric oxide donor. The same variables were also monitored in: (a) rats fed a threonine free diet and injected with saline; (b) animals fed a standard diet and injected with nitroprusside; (c) rats fed a standard diet and injected with saline. The results showed that the threonine-free diet reduced food intake and GLU and ASP concentrations in the accumbens. NP reduced the hypophagia, but it did not change GLU and ASP levels in rats fed the threonine-free diet. In animals fed the standard diet, NP increased GLU and ASP concentration, and food intake. No change was found in the animals with saline injection. These findings suggest that nitric oxide reduces the hypophagia in the rats fed a threonine-free diet. The lack of increase in GLU and ASP concentration in the nucleus accumbens of the hypophagic rats indicates that NP acts on hypophagia independently by GLU and ASP.

Aspartic and glutamic acids increase in the frontal cortex during prostaglandin E1 hyperthermia.

The aim of the present experiment was to evaluate the role played by aspartic acid and glutamic acid of frontal cerebral cortex during the hyperthermia induced by prostaglandin E1. Two groups of six Sprague Dawley male rats were anaesthetized with ethyl-urethane. The frontal cortical concentrations of aspartic and glutamic acids, the firing rate of the sympathetic nerves to the interscapular brown adipose tissue, the colonic and interscapular brown adipose tissue temperatures were monitored both before and after an intracerebroventricular injection of prostaglandin E1 (500 ng) or saline. Aspartic and glutamic acids were collected using a microdialysis probe placed in the frontal cortex. Concentrations of aspartic and glutamic acids were measured by high-pressure liquid chromatography with fluorescence detector. Prostaglandin E1 induced an increase in the concentrations of aspartic and glutamic acids, in the firing rate of sympathetic nerves and in the colonic and interscapular brown adipose tissue temperatures. The findings of the present experiment indicate that an intracerebroventricular injection of prostaglandin E1 causes release of aspartic and glutamic acids in the frontal cortex.

Procaine injection into the paraventricular nucleus reduces sympathetic and thermogenic activation induced by frontal cortex stimulation in the rat.

These experiments were designed to test the effect of procaine injection into the paraventricular nucleus on the sympathetic and thermogenic changes induced by frontal cortex stimulation. Oxygen consumption, firing rate of the sympathetic nerves to interscapular brown adipose tissue (IBAT), along with IBAT and colonic temperatures (T(IBAT) and T(C)) were monitored in fasted male Sprague-Dawley rats before and 25 min after an electrical stimulation of the frontal cortex. The same variables were monitored in rats with administration of procaine into the paraventricular nucleus. The results show that cortical stimulation raises oxygen consumption, sympathetic neuron firing rates, T(IBAT), and T(C). This increase is reduced by procaine injection. These findings suggest that the paraventricular nucleus plays a key role in the sympathetic and thermogenic changes induced by cortical stimulation.

The effect of a carbohydrate loading on running performance during a 25-km treadmill time trial by level of aerobic capacity in athletes.

The aim of the present study was to examine the influence of a high carbohydrate diet and the level of aerobic capacity on running performance during a 25-km treadmill time trial. The study used a 2*2 design with the factors being training and diet composition. We divided the athletes in 4 groups: 1. Trained athletes with carbohydrate loading (CHO1); 2. Trained athletes without carbohydrate loading (C1); 3. Untrained athletes with carbohydrate loading (CHO2); 4. Untrained athletes without carbohydrate loading (C2). The carbohydrate loading was effected with confectionery. Performance time, running speed, blood glucose and blood lactate concentrations were evaluated during two 25-km treadmill time trial (trial 1 and trial 2) separated by 7 days in which two groups (CHO1 and CHO2) had a carbohydrate loading. The results showed that the athletes with lower level of aerobic capacity had better performance time after carbohydrate loading. They ran faster and had a higher glucose and lactate concentrations in the last 5 km during trial 2. There were no significant differences in the other groups. In conclusion, we can assert that dietary carbohydrate loading can improve running performance and that confectionery can be used as an effective means of supplementing the normal carbohydrate intake in preparation for endurance competitions. But the improvement depends on some factors such as the distance and the level of aerobic capacity.

L-threonine injection into PPC modifies food intake, lateral hypothalamic activity, and sympathetic discharge.

Food intake and the firing rate of lateral hypothalamic neurons and nerves innervating interscapular brown adipose tissue (IBAT), along with IBAT and colonic temperatures, were monitored in male Sprague-Dawley rats fed a threonine-free diet. These variables were measured before and after a bilateral injection of L-threonine (2 nmol into each side) into the prepiriform cortex (PPC). The same variables were also monitored in 1) rats fed a threonine-free diet and injected with saline, 2) animals fed a standard diet and injected with L-threonine, and 3) rats fed a standard diet and injected with saline. The results showed that injection of L-threonine into PPC increases food intake and firing rate of lateral hypothalamic neurons, whereas it decreases the sympathetic discharge and body temperature in animals fed a threonine-free diet. No changes were found in the animals fed a standard diet. These findings suggest a correlation between 1) threonine level in the PPC and 2) lateral hypothalamic activity and sympathetic discharge to IBAT.

Lesions of the ventromedial hypothalamus reduce postingestional thermogenesis.

The aim of this experiment was to evaluate the effects of ventromedial hypothalamus lesions on the thermogenic changes that follow food intake. Four groups of six Sprague-Dawley male rats were used. Under anesthesia with pentobarbital, the animals in the first and second groups received lesions at the ventromedial hypothalamus, and animals in the third and fourth groups received sham lesions. Body weight and food intake were monitored daily until the experimental procedure began. Twenty days after lesion, oxygen consumption, firing rate of sympathetic nerves to interscapular brown adipose tissue (IBAT), and IBAT temperature were monitored for 45 min both before and after 5 g food intake in 24 h fasted rats from the first and third groups. The same variables were measured in the animals of the second and fourth groups 50 days after receiving the lesions. Lesion placements were histologically verified. The results showed that lesions produced hyperphagia and obesity. Firing rate of nerves to IBAT, IBAT temperature, and oxygen consumption increased after food intake in sham-lesioned rats. This increase was significantly reduced by the lesion at both the 20- and 50-day time points. These findings indicate that the ventromedial hypothalamus controls postingestional activation of sympathetic discharge to IBAT. The reduction of postingestional thermogenesis could be involved in the development of obesity induced by lesion of the ventromedial hypothalamus.

Acute lesions of the ventromedial hypothalamus reduce sympathetic activation and thermogenic changes induced by PGE1.

The aim of this experiment was to evaluate the effects of an intracerebroventricular (icv) injection of prostaglandin E1 (PGE1) on the sympathetic activation and the thermogenic changes in rats with acute lesions of the ventromedial hypothalamus (VMH). Four groups of six Sprague-Dawley male rats were anesthetized with ethyl-urethane. The firing rate of the sympathetic nerves innervating the interscapular brown adipose tissue (IBAT) and the colonic and IBAT temperatures were monitored both before and after one of the following treatments: 1) VMH lesion plus icv injection of PGE1 (500 ng); 2) VMH lesion plus icv injection of saline: 3) sham lesion plus icv injection of PGE1; and 4) sham lesion plus icv injection of saline. PGE1 induced an increase in the firing rate of IBAT nerves and the colonic and IBAT temperatures. These effects were reduced by VMH lesion. The findings indicate that acute lesions of the VMH reduce the effects of PGE1 and seem to suggest a possible role played by the VMH in the control of the sympathetic activation and the thermogenic changes during PGE1 hyperthermia.

Lysine acetylsalicylate modifies aphagia and thermogenic changes induced by lateral hypothalamic lesion.

These experiments test the effect of intraperitoneal injection of lysine acetylsalicylate on 1) food intake and 2) the sympathetic and thermogenic changes induced by lesion of the lateral hypothalamus (LH). Food intake, firing rate of the nerves innervating interscapular brown adipose tissue (IBAT), and IBAT and colonic temperatures (TIBAT and TC) were monitored in male Sprague-Dawley rats lesioned in the LH. These variables were measured before and after intraperitoneal injection of lysine acetylsalicylate. The same variables were also monitored in 1) lesioned rats with intraperitoneal administration of saline, 2) sham-lesioned animals with intraperitoneal injection of lysine acetylsalicylate, and 3) sham-lesioned rats with intraperitoneal injection of saline. The results show that lysine acetylsalicylate modifies the aphagia by increasing food intake and also reduces the enhancements in firing rate, TIBAT, and TC induced by LH lesion. These findings suggest that prostaglandin synthesis plays a key role in the control of eating behavior in LH-lesioned rats by acting on the sympathetic and thermogenic changes induced by LH lesion.

Lateral hypothalamic lesion induces sympathetic stimulation and hyperthermia by activating synthesis of cerebral prostaglandins.

This experiment tests the effect of intracerebroventricular (icv) injection of lysine acetylsalicylate on the sympathetic and thermogenic changes induced by lesion of the lateral hypothalamus (LH). The firing rate of the nerves innervating interscapular brown adipose tissue (IBAT), along with IBAT and colonic temperatures (TIBAT and Tc) were monitored in urethane-anaesthetized male Sprague-Dawley rats lesioned in the LH. These variables were measured before and after an icv injection of 1mg lysine acetylsalicylate. The same variables were also monitored in: a) lesioned rats with icv administration of saline; b) sham-lesioned animals with icv injection of lysine acetylsalicylate; c) sham-lesioned rats with icv injection of saline. In an additional experiment, the same variables were monitored after an icv injection of lysine acetylsalicylate or saline in rats with LH lesion performed 48 h before the icv injection. The results show that lysine acetylsalicylate injection reduces the increases in firing rate, TIBAT and Tc induced by LH lesion. These findings suggest that cerebral prostaglandin synthesis plays a key role in the sympathetic and thermogenic changes following LH lesion.

NG methyl-L-arginine increases the hyperthermic effects of prostaglandin E1.

The sympathetic firing rate of the nerves innervating interscapular brown adipose tissue (IBAT), IBAT and colonic temperatures (TIBAT and TC) were monitored in urethane-anaesthetized male Sprague-Dawley rats. These variables were measured for a period of 40 min before (baseline values) and 40 min after a 2 mg NG-methyl-L-arginine (NMA) injection plus an intracerebroventricular administration of 500 ng prostaglandin E1 (PGE1) into a lateral cerebral ventricle. No drug was injected in control rats. The results show that NMA enhances the increases in firing rate, TIBAT and TC induced by PGE1. These findings indicate that an inhibitor of nitric oxide synthesis, such as NMA, increases the sympathetic and thermogenic responses to injection of PGE1.

Changes in eating behavior and thermogenic activity following inhibition of nitric oxide formation.

The effects of the inhibition of nitric oxide (NO) production on eating behavior and thermogenesis were evaluated in the present experiments. NG-nitro-L-arginine methyl ester (L-NAME), an inhibitor of NO production, was injected intraperitoneally or intracerebroventricularly, and food intake, oxygen consumption rate, and interscapular brown adipose tissue (BAT) temperature were evaluated in conscious rats. The firing rate of sympathetic nerves innervating interscapular BAT was recorded in urethan-anesthetized animals. L-NAME, intraperitoneally injected, decreased food intake, oxygen consumption, temperature, and firing rate of sympathetic nerves innervating interscapular BAT. Intracerebroventricular injection of L-NAME decreased food intake and enhanced oxygen consumption, temperature, and firing rate of sympathetic nerves innervating BAT. The latter changes were similar to those found after lateral hypothalamic lesions. The opposite changes in oxygen consumption, temperature, and sympathetic activity of BAT that followed L-NAME injection through the two different routes were probably due to different effects of the molecule on sympathetic output. Impaired brain production of NO, which followed intracerebroventricular L-NAME, directly increased sympathetic activity, whereas the same activity that followed intraperitoneal L-NAME was depressed by increased blood pressure, which was elicited by the impaired peripheral production of NO.

Nitric oxide reduces body temperature and sympathetic input to brown adipose tissue during PGE1-hyperthermia.

The firing rate of the nerves innervating interscapular brown adipose tissue (IBAT) and IBAT and colonic temperatures (TIBAT and TC were monitored in urethane-anaesthetized male Sprague-Dawley rats. These variables were measured for 40 min before (baseline values) and 40 min after a 4 micromoles L-arginine (L-arg) or 400 nmoles nitroprusside (NP) injection in a lateral cerebral ventricle and an intracerebroventricular administration of 500 ng prostaglandin E1 (PGE1). The same variables were monitored in other rats with L-arg or NP or PGE1 administration alone. No drug was injected in control rats. The results show that L-arg or NP injection reduces the increases in firing rate, TIBAT, Tc induced by PGE1. These findings suggest that nitric oxide is important in the control of thermogenic changes during the PGE1 hyperthermia.