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In affluent societies high caloric intake and chronic stress are currently associated with upper body fat. We investigated the effects of a high-sucrose (S) diet and dexamethasone (DEX) on fat depots (experiment 1) and lipid fuel fluxes (experiment 2) in male Wistar rats. In experiment 1, a liquid diet of commercial powdered milk containing 31% calories as carbohydrate or an isocaloric S diet (80% calories as carbohydrate) was offered to male rats. One half of the rats on each diet received a daily dose of 3 microg DEX in their diet. Intake was measured daily and body weight 3 times a week. Rats were killed after 7 weeks, and fat depot weights and carcass lipid were determined. In a second experiment, other rats received only the S diet with or without DEX. After 7 weeks, under pentobarbital anesthesia, arterial, portal, and iliolumbar vein blood was drawn, and the liver was extracted. Plasma concentration of triacylglycerides (TAG), nonesterified fatty acids (NEFA), glycerol (GOL), and lactate (L) and liver TAG were measured. Rats on the S diet ingested less and gained less weight. DEX treatment significantly reduced body weight gain. All fat depots as percentage of body weight were increased only in the S-DEX group. The S-DEX group had more liver TAG and less arterial NEFA and GOL than the S group. TAG determinations showed unexpected results: portal levels in the S-DEX group and iliolumbar levels in both groups were significantly higher than in the arterial plasma. This fact, together with high NEFA/GOL ratios in these veins, may signify incomplete TAG hydrolysis by lipoprotein lipase. L levels were higher in the S-DEX group and higher in arterial versus venous blood in both groups, indicating L uptake both in the splanchnic area and the retroperitoneal fat. These results show that, in rats, a long-term high-sucrose diet has peculiar effects on L turnover, and when associated with DEX, it also increases fat depots, induces liver steatosis, and, presumably, inhibits complete hydrolysis of TAG by lipoprotein lipase (LPL).

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Paraganglia are clusters of cells containing catecholamines (CA), mainly norepinephrine (NE) and dopamine (DA). The presence of epinephrine (E), on the other hand, has only been determined by indirect methods in retroperitoneal paraganglia of newborn and aged rats. Because their location, paraganglia associated with the hepatic branch of the vagus nerve may be a possible source of CA for the liver. The main purposes of the present study were to determine CA levels and whether E can be found in the omentum minus which includes paraganglia associated with the hepatic branch of the vagus nerve, and then to study the effects of 6-hydroxydopamine and reserpine on their CA content. Twenty-four female Wistar rats were randomly ascribed to three groups receiving two intraperitoneal injections of either 6-hydroxydopamine, reserpine or saline. Twenty-four hours after the last administration the rats were anesthetized and a portion of the omentum minus was obtained. Left adrenal medulla and a liver fragment were also collected as controls. The samples were processed to be analyzed by high performance liquid chromatography and catecholamine histofluorescence. The results confirm previous reports about the presence of considerable amounts of norepinephrine and dopamine in paraganglia. Norepinephrine and dopamine in the omentum like the adrenal medulla were significantly depleted by reserpine but not by 6-hydroxydopamine treatment, suggesting that some other sources in addition to sympathetic terminals are responsible for CA in the omentum. On the contrary, both drugs reduced liver NE, consistent with the localization of this amine mainly to hepatic sympathetic terminals. Histofluorescence of the omentum revealed 2-4 paraganglia per tissue fragment. Paraganglia associated with the hepatic branch of the vagus nerve contain also E. The presence of perihepatic sources of extra-adrenal CA, and more specifically E, could be of physiological significance.

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In previous works it was shown that catecholamine-induced hypodipsia is mediated by alpha1-adrenergic receptors while food intake (FI) inhibition supposes also beta-adrenergic participation. We used sodium nitroprusside (N) as a vasodilator, alone or mixed with various adrenergic agonists and measured FI and water intake (WI) in rats either deprived food and water overnight or in postprandial conditions after only 1 hour of deprivation in day time. N injected alone had no effect after overnight deprivation but diminished significantly norepinephrine (NE)-induced inhibition of both intakes, while epinephrine (E) inhibited only FI. In day time, N stimulated 30 min FI by 60% and WI by 84% in male but not in female rats. Isoproterenol (I) stimulated only WI (by 155%), while phenylephrine (P) and E inhibited it by 55%. In the presence of N, I increased WI even more (by 220%) but reduced FI. P + N and E + N increased FI by 41% and 128% as compared with P and E, respectively. Only P-induced inhibition of WI was canceled in presence of N. The results show that N, probably due to nitric oxide production, may induce hyperphagia and hyperdipsia in 1 hour-deprived male rats and also that catecholamine effects on FI and WI are differently modulated by N.

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Intraperitoneal (IP) fat accumulation in humans is a risk factor for a number of diseases. We tried to increase this particular adipose mass in rats by long-term administration of low-dose dexamethasone (Dex) and/or elimination of other fat depots. Male adult Wistar rats were lipectomized (Lip) or sham-operated (Sh). Bilateral lipectomy of retroperitoneal and inguinal fat pads was performed under anesthesia with Na pentobarbital 40 mg/kg supplemented with ether. After 8 days, half the animals of each group received Dex in their drinking water (0.1 microgram/mL) while the other half received water (W), for a total of four groups: Sh-W, Lip-W, Sh-Dex, and Lip-Dex. Body weight (BW) and food and water intake were measured throughout the treatment period. A glucose tolerance test was performed 34 days after starting Dex treatment, and then rats were killed, fat depots were weighed, and plasma and liver were obtained for metabolic determinations. Dex rats ate the same amount of food as W controls, but gained significantly less weight (2.02 +/- 0.18 v 3.82 +/- 0.10 g/d, P < .01). Mean daily W intake was approximately 40 mL/d in all groups, which means that Dex rats ingested approximately 4 micrograms/d Dex. Average glycemic values during the 180-minute glucose tolerance test were as follows: Sh-W, 162 +/- 13; Lip-W, 166 +/- 7; Sh-Dex, 118 +/- 6; and Lip-Dex, 229 +/- 27 mg/dL. These values show that glucose tolerance was improved by Dex treatment alone, but was impaired in Lip-Dex animals. The same trend was evident for the relative weights (percent of BW) of two intact adipose depots: IP and epididymal (EPI) (Sh-W, 2.08 +/- 0.13 and 1.35 +/- 0.11, respectively; Lip-W, 1.67 +/- 0.15 and 1.17 +/- 0.11; Sh-Dex, 1.66 +/- 0.10 and 1.28 +/- 0.07; Lip-Dex, 2.41 +/- 0.11 and 1.53 +/- 0.09). Average glycemia for all rats was significantly correlated with IP (r = .55, P < .01) but not with EPI; moreover it was correlated in the Sh-W control group (r = .81, P < .05), suggesting a normal relation between these variables. Liver triglycerides (LTG), which were elevated in Dex rats, were also correlated with IP (r = .51, P < .02 for all rats and r = .82, P < .05 for Sh-W rats). The results show that long-term administration of low-dose Dex has some different effects in normal versus Lip rats concerning mainly the IP fat depot, the relative mass of which seems to significantly affect glucose tolerance.

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UNLABELLED: In a previous publication we showed that intraperitoneally (IP) injected norepinephrine (NE) induces hypodipsia (hD) in rats by an alpha 1-adrenergic effect which might be due to splanchnic vasoconstriction. In the present work we administered two vasoconstrictive hormones: NE 250 ug/kg and arginine vasopressin (VP) 550 mU/kg either by IP or intramuscular (IM) route to fasted rats in two different thirst-inducing conditions: (a) water-deprivation; or (b) induced hyperosmolarity. IP NE inhibited significantly food and water intake under both conditions. IM NE did not affect food intake and elicited significantly less hD and this only in (a). VP did not affect food intake but induced hD regardless of the route of administration in (a) but not in (b). NE administrated to anesthetized rats after food and water deprivation increased arterial pressure by both routes while VP effect was weaker and more variable. IN CONCLUSION: blood pressure elevation may be implicated in the hD effect but IP NE elicits a specific splanchnic action; splanchnic-induced hypophagia is not necessarily related to water intake inhibition.

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Oxygen consumption (VO2), carbon dioxide production (VCO2), the resulting respiratory quotient (RQ), and motor activity were recorded simultaneously by an on-line computer every ten seconds during 16-20 hours in two decerebrate male rats. Being aphagic and adipsic the rats were fed twice daily by gastric intubation with a mixture of powdered milk plus sugar or plus sunflower oil (approx. 300 KJ daily) in 10-20 ml tap water. In all seven tests performed on these rats the recordings presented very steep reductions of RQ due every time to steep increases in VO2 without increases in VCO2. Mean number of VO2 peaks in all experiments was 12.4 +/- 1.8 (SE) with mean duration of 21.3 +/- 2.8 min. Two normal male rats were fed the same diet and on the same schedule: they presented similar VO2 peaks in 8 out of 12 experiments. Mean number was 8.7 +/- 1.0 with mean duration of 13.6 +/- 2.2 min. The VO2 peak periods never occurred in rats fed ad libitum. In the two normal rats oil ingestion produced more effect than sugar. It is suggested that the phenomenon could be due to a metabolic imbalance possibly of hepatic origin, more evident in decerebrate rats. VO2 peaks could be produced by enhanced ketogenesis, gluconeogenesis and/or extra-mitochondrial (peroxisomal, microsomal) oxidation.

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