Satiety and memory enhancing effects of a high-protein meal depend on the source of protein.

OBJECTIVE: High- protein diets have become increasingly popular with various touted benefits. However, the extent to which protein quantity and source affects cognitive functioning through altering postprandial amino acid profiles has not been investigated. Further, whether all protein sources are similarly anorexigenic is uncertain. The objective of this study was to determine the influence of protein level and source on Barnes maze performance, satiety and plasma amino acid levels in male Sprague-Dawley rats. METHODS: Rats were entrained to a meal-feeding schedule consisting of a 30 minutes meal, equivalent to 20% of average daily intake, one hour into the dark phase then ad libitum access to food for 5 h. On test days, rats received one of three isocaloric diets as their first meal, hereafter referred to as Egg White (EW), Wheat Gluten (WG), or Basal, and then were measured for cognitive performance, feeding behavior, or plasma amino acid levels via jugular catheter. Percentage energy from protein was 35% for both EW and WG and 20% for Basal with equal amounts provided by EW and WG proteins. RESULTS: Rats provided EW performed similarly to Basal on the Barnes maze, whereas WG performed worse. EW increased satiety, whereas WG reduced satiety relative to Basal. Both EW and WG increased postprandial concentrations of large neutral and branched chain amino acids relative to Basal, but in EW, concentrations were slower to peak, and peaked to a higher level than WG. DISCUSSION: Results demonstrate the importance of protein source for cognition and satiety enhancing effects of a high-protein meal.

Rate of fall in blood glucose and recurrent hypoglycemia affect glucose dynamics and noradrenergic activation in the ventromedial hypothalamus.

Noradrenergic activity in the ventromedial hypothalamus (VMH) is increased and activates a sympathoadrenal response during hypoglycemia. How the rate at which hypoglycemia develops affects local glucose concentrations and norepinephrine (NE) release was evaluated by placing microdialysis probes into the VMH of male Sprague-Dawley rats receiving insulin (20 mU·kg(-1)·min(-1)) and variable glucose infusions. During a first episode of hypoglycemia, interstitial glucose concentrations in the VMH generally declined at the same rate as plasma glucose; however, the faster hypoglycemia developed, the greater the magnitude of the initial NE release in the VMH (r(2) = 0.72, P < 0.001). Following recurrent episodes of hypoglycemia, VMH glucose decreased at a slower rate than plasma glucose, and the initial NE release was attenuated at the same rates of blood glucose decline. The plasma glucose threshold for the initial NE release in VMH was similar for all groups (∼3.23 mM); however, the VMH glucose threshold was stimulated and was lower when blood glucose declined more slowly (0.86 ± 0.06 vs. 1.06 ± 0.04 mmol/l, P < 0.01). The timing of the initial increase in NE release in VMH corresponded with an increase in plasma epinephrine during the first episode of hypoglycemia but not following recurrent hypoglycemia. Although a decrease in VMH glucose concentration is required for noradrenergic activation in VMH, there does not appear to be a set glucose threshold within the VMH for activation of this response.

Intracerebroventricular administration of soy protein hydrolysates reduces body weight without affecting food intake in rats.

Some studies suggest that increased consumption of soy protein hydrolysates may cause body weight loss but the mechanism of action is unknown. The objective of this investigation was to determine whether intracerebroventricular (i.c.v.) infusion of soy protein hydrolysates decrease food intake and body weight. Adult male Sprague Dawley rats (n = 24) received i.c.v. injections of soy hydrolysate I (SH I) or soy hydrolysate II (SH II) three times weekly for 2 weeks. Krebs solution and leptin were used as negative and positive controls respectively. SH I (6.5-20 kDa with a strong band at 14 kDa) was produced by hydrolysis with alcalase, and SH II (approximately 2 kDa) was obtained by hydrolysis and ultrafiltration. Leptin successfully reduced body weight (-1.60 g) 24 h (p = 0.0093) after the third injection. SH I caused significant (p = 0.0009) decreases in body weight (-1.70 g) 24 h after the third injection but not after 48 h. SH II showed a tendency to prevent body weight gain but this effect was short of statistical significance (p < 0.40). Food intake was not affected by any of the soy hydrolysate treatments but leptin injection did cause significant decreases in food intake (p < 0.05). Data suggest that soy alcalase hydrolysate can decrease, in the short term, the rate of body weight gain independently of food consumption. This preliminary data show that soy peptides may play a role on body weight regulation, possibly by increasing energy utilization.

Orexin-induced feeding requires NMDA receptor activation in the perifornical region of the lateral hypothalamus.

Food intake is stimulated following administration of orexin-A into the perifornical region of the lateral hypothalamus (LH/PFA). Orexin neurons originating in the LH/PFA interact with a number of hypothalamic systems known to influence food intake, including glutamatergic neurons. Glutamatergic systems in the LH/PFA were demonstrated to initiate feeding through N-methyl-d-aspartic acid (NMDA) receptors. Male Sprague-Dawley rats fitted with brain guide cannulas to the LH/PFA were used in two experiments. In the first experiment, a combination microdialysis/microinjection probe was used to deliver artificial cerebrospinal fluid (aCSF) or 500 pmol of orexin-A into the LH/PFA. Orexin-A increased interstitial glutamate to 143 +/- 12% of baseline (P < 0.05), which remained elevated over the 120-min collection period. In the second experiment, the NMDA receptor antagonist d-2-amino-5-phosphonopentanoic acid (d-AP5; 10 nmol) was administered before orexin-A. The orexin-induced increase in food intake (from 1.1 +/- 0.4 to 3.2 +/- 0.5 g, P < 0.05) during the first hour was absent in rats receiving d-AP5 + orexin-A (1.2 +/- 0.5 g). There was no effect of d-AP5 alone on food intake. These data support glutamatergic systems in the LH/PFA mediating the feeding response to orexin-A through NMDA receptors.

Noradrenergic activity in the paraventricular nucleus and macronutrient choice during early dark onset by zinc deficient rats.

Carbohydrate is a preferred macronutrient of rats during the early dark phase and associated with an increase in norepinephrine (NE) and neuropeptide Y (NPY) in the paraventricular nucleus (PVN). Macronutrient choice is altered during zinc deficiency (ZD). The relationship between NE activity in the PVN and macronutrient choice during early dark was evaluated in rats fed zinc adequate (ZA) or ZD diet for 14 days. Total caloric intake was similar for ZA and ZD groups (-20 kJ) but ZA rats selected 63 +/- 5% of calories as carbohydrate while ZD rats selected 53 +/- 5% of their calories from protein (p < 0.01). Pair-fed (PF) rats selected 62 +/- 5% of calories as carbohydrate. Noradrenergic activity was lower (p < 0.01) in ZD and PF compared to ZA. The association between increased NE in the PVN at dark onset and selection of carbohydrate is not supported by the present results.

Hypoglycemia-induced noradrenergic activation in the VMH is a result of decreased ambient glucose.

During insulin-induced hypoglycemia, there is an increase in extracellular norepinephrine (NE) in the ventromedial hypothalamus (VMH). This brain area is known to play an important role in integrated hormonal and behavioral responses to systemic hypoglycemia. Selective glucoprivation restricted to the VMH is both necessary and sufficient to initiate secretion of counterregulatory hormones. The present study was designed to investigate whether increased release of NE in the VMH depends on detection of glucoprivation localized in this area. In awake, chronically catheterized male Sprague-Dawley rats, extracellular NE in the VMH was monitored using 1-mm microdialysis probes perfused with Krebs Ringer buffer (KRB) or KRB + 100 mM d-glucose (d-Glc). During insulin-induced hypoglycemia (glycemic nadir approximately 2.4 mM) extracellular NE was increased to >160% of baseline (P < 0.01) only in the KRB + insulin group. There was no increase in NE from baseline when glucose was added to the perfusate to maintain euglycemia at the periprobe environment. The sympathoadrenal response to hypoglycemia, present in the KRB + insulin group, was attenuated in the d-Glc + insulin group. The present results confirm that noradrenergic activation in the VMH during systemic hypoglycemia depends on detection of glucoprivation locally in this area. These data provide additional support for the importance of increased noradrenergic activity in the VMH in the counterregulatory hormonal responses to hypoglycemia.

Effect of the estrous cycle on water maze acquisition depends on the temperature of the water.

The literature on the effects of ovarian hormones on rodent learning and memory is mixed. In this study, the authors examined the role of task stressfulness. Female hooded rats were tested during proestrus or estrus on the hidden-platform water maze in warm (33 degrees C) or cold (19 degrees C) water. There were no effects of cycle or temperature, but estrous phase interacted with temperature such that proestrous rats performed better overall under the warm condition and estrous rats performed better under the cold condition. Plasma corticosterone, measured after 4 trials, varied significantly with estrous phase. Water temperature, perhaps through stress, influences the effect of estrous phase on water maze performance.

Dissociation of hypothalamic noradrenergic activity and sympathoadrenal responses to recurrent hypoglycemia.

This study evaluated whether attenuation of sympathoadrenal responses to recurrent hypoglycemia is mediated by diminished noradrenergic activity in the hypothalamus. Male Sprague-Dawley rats received either once daily insulin (1.0 units/kg) injections or an equal administration of saline for 3 days. Both groups received an administration of insulin on the fourth day, during which blood glucose and plasma catecholamines were determined, and extracellular norepinephrine (NE) in the ventromedial hypothalamus (VMH) or paraventricular hypothalamic nucleus (PVN) was monitored with microdialysis. The peak response of plasma epinephrine to insulin-induced hypoglycemia (nadir approximately 3.2 mmol/l) was significantly reduced during the fourth hypoglycemic episode (774 +/- 134 pg/ml) compared with the first episode (2,561 +/- 410 pg/ml, P < 0.001). Baseline levels of extracellular NE were elevated approximately 25% (P = 0.07) in the VMH and approximately 46% (P = 0.03) in the PVN after multiple hypoglycemic episodes. There was no difference in noradrenergic activity during the first or fourth hypoglycemic episode in either brain area. The reduced sympathoadrenal output after recurrent hypoglycemia is likely postsynaptic from hypothalamic NE release or is mediated via a collateral pathway.

Zinc status affects neurotransmitter activity in the paraventricular nucleus of rats.

Alterations in neurochemical activity in the paraventricular nucleus (PVN) of the hypothalamus may account for decreased intake of zinc-deficient diets. Male Sprague-Dawley rats were fed zinc-deficient (ZD) or zinc-adequate (ZA) diet for 14 d before samples of extracellular fluid in the PVN were collected by microdialysis or push-pull perfusion. A third set of rats was pair-fed (PF) an amount of ZA diet equal to the intake of ZD rats. Samples were collected over a 2-h period spanning the transition from light to dark. All rats then consumed the zinc adequate diet ad libitum for 3 d before a second set of samples was collected. The increase in extracellular norepineprhrine (NE) during h 1 of the dark period to 147 +/- 13% of baseline (P < 0.05) was apparent only in ZA rats at d 14. After the 3-d repletion period, the increase in NE at dark onset occurred in all three groups. An increase in extracellular neuropeptide Y (NPY) at dark onset to 174 +/- 32% of baseline in rats fed ZA (P < 0.01) was measured in all three groups at both d 14 and 17. Basal NPY concentrations were significantly elevated in PF rats on d 14 (7.45 +/- 2.01 vs. 0.58 +/- 0.23 pmol/L, P = 0.01) and returned to ZA levels by d 17. The activities of the NE and NPY systems in the PVN were altered in rats fed a zinc-deficient diet; however, it is unclear whether the disruption in the NE and NPY neural systems in the PVN results in the altered feeding behavior accompanying zinc deficiency.