Postprandial variations of plasma inflammatory markers in abdominally obese men

Objective: Abdominal obesity is associated with a fasting proinflammatory condition. However, not much is known of the potential variations in circulating inflammatory markers after food intake. The purpose of the present study was to examine postprandial changes in plasma tumor necrosis factor (TNF)‐α, interleukin (IL)‐6, and C‐reactive protein (CRP) concentrations in men and their potential associations with fat distribution and metabolic profile variables. Research Methods and Procedures: Thirty‐eight men were given a high‐fat meal in the morning after an overnight fast, and TNF‐α, IL‐6, and CRP levels were measured in plasma at 0, 4, and 8 hours after the meal. Physical and metabolic profiles were also assessed for each participant. Results: We observed a substantial increase in circulating IL‐6 levels (p < 0.0001) after the meal. Although postprandial variations in circulating TNF‐α levels across time failed to reach statistical significance (p = 0.02), we noted a significant decrease in plasma TNF‐α concentrations 4 hours (?10%, p < 0.001 vs. 0 hours) after food intake. Plasma CRP levels were not affected by the fat load. We also noted that insulin‐sensitive individuals displayed a less pronounced inflammatory response after food intake than insulin‐resistant subjects. Discussion: Results of the present study show that consumption of a high‐fat meal leads to an increase in plasma IL‐6 concentrations and transient decrease in circulating TNF‐α levels in overweight men. Our results suggest a possible role of insulin resistance in the modulation of the postprandial inflammatory response, which could, in turn, contribute to worsen the state of insulin resistance.     

Effect of Enterostatin on the Feeding Responses to Galanin and NPY

We have investigated the possibility that enterostatin may inhibit the intake of dietary fat by inhibiting either galanin or NPY-induced feeding pathways. Rats, adapted to either high fat (HF) or low fat-high carbohydrate (HC) diets and fitted with third ventricular cannulas were used to study the effects of intracerebroventricular (icv) enterostatin on icv NPY and galanin induced feeding responses in satiated rats. An equimolar dose of enterostatin (0.1nmoles) inhibited, while a tenfold excess of entersotatin abolished the feeding response to galanin in rats adapted to a HF diet. The galanin stimulation of food intake was reduced in rats adapted to the HC diet and this response was less sensitive to inhibition by enterostatin. Enterostatin had no inhibitory effects on NPY-induced feeding in rats adapted to the HC diet and only a small inhibitory effect, at tenfold molar excess, in rats adapted to the HF diet. The ability of enterostatin to bind to galanin or NPY Y-1 receptors was investigated in lig and binding studies. Enterstatin fialed to dispace ¹²⁵I-galanin or ¹²⁵I-PYY from specific binding sites in rat forebrain homogenates or SK-N-MC cells respectively. The data provide support for the hypothesis that enterostatin specifically inhibits a galanin-responsive fat intake system, but indicate that this effect is not modulated by direct interaction with either galanin or NPY-Y1 receptors.     

High‐Fat Diet Feeding Elevates Skeletal Muscle Uncoupling Protein 3 Levels But Not Its Activity in Rats

Objective: The objective of this study is to test the impact of high‐fat diet (HFD) feeding on skeletal muscle (SM) uncoupling protein 3 (UCP3) expression and its association with mitochondrial ion permeability and whole‐body energy homeostasis. Research Methods and Procedures: Sprague–Dawley rats were fed ad libitum either a HFD (60% of energy from fat, n = 6) or a low‐fat diet (12% of energy from fat, n = 6) for 4 weeks. Twenty‐four‐hour energy expenditure was measured by indirect calorimetry in the last week of the dietary treatment. Blood samples were collected for plasma leptin and free fatty acid assays, and mitochondria were isolated from hindlimb SM for subsequent determinations of UCP3 levels and mitochondrial ion permeability. Results: Plasma leptin levels were higher in rats fed the HFD despite the same body weight in two groups. The same dietary treatment also rendered a 2‐fold increase in plasma free fatty acid and SM UCP3 protein levels (Western blot) compared with the group fed the low‐fat diet. However, the elevated UCP3 protein levels did not correlate with mitochondrial swelling rates, a measure of mitochondrial chloride, and proton permeability, or with 24‐hour energy expenditure. Discussion: The high correlation between the levels of plasma free fatty acid levels and SM UCP3 suggests that circulating free fatty acid may play an important role in UCP3 expression during the HFD feeding. However, the dissociation between the UCP3 protein levels and 24‐hour energy expenditure as well as mitochondrial ion permeability suggests that mitochondrial proton leak mediated by muscle UCP3 may not be a major contributor in energy balance in HFD feeding, and other regulatory mechanisms independent of gene regulation may be responsible for the control of UCP3‐mediated uncoupling activity.     

Effects of Dinner Composition on Postprandial Macronutrient Oxidation in Prepubertal Girls

Objective: To see whether a fat‐rich (50%) evening meal promoted fat oxidation and a different spontaneous food intake on the following day at breakfast than a meal with a lower fat content (20%) in 10 prepubertal obese girls. Research Methods and Procedures: The postabsorptive and postprandial (10.5 hours) energy expenditure after a low‐fat (LF) (20% fat, 68% carbohydrate, 12% protein) and an isocaloric (2.1 MJ) and isoproteic high‐fat (HF; 50% fat, 38% carbohydrate, 12% protein) meal were measured by in direct calorimetry. Results: Fat oxidation was not significantly different after the two meals [LF, 31 ± 9 vs. HF, 35 ± 9 g/10.5 hours, p = not significant (NS)]. The girls oxidized 1.8 ± 0.9 times more fat than that ingested (11.1 grams) with the LF meal vs. 0.3 ± 0.3 times more fat than that ingested (27.1 grams) with the HF meal (p < 0.001). Carbohydrate oxidation was significantly higher after an LF than an HF meal (39 ± 12 vs. 29 ± 9 g/10.5 hours, p < 0, 05). At breakfast, the girls spontaneously ingested a similar amount of energy (1.5 ± 0.7 vs. 1.5 ± 0.6 MJ, p = NS) and macronutrient proportions (fat, 23% vs. 26%, p = NS; protein, 9% vs. 10%; carbohydrate, 68% vs. 64%,) independently of their having eaten an HF or an LF dinner. Discussion: An HF dinner did not stimulate fat oxidation, and no compensatory effect in spontaneous food intake was observed during breakfast the following morning. Cumulated total fat oxidation after dinner was higher than total fat ingested at dinner, but a much larger negative fat balance was observed after the LF meal. Spontaneous energy and nutrient intakes at breakfast were similar after LF and HF isocaloric, isoproteic dinners. This study points out the lack of sensitivity of short‐term fat balance to subsequently readjust fat intake and emphasizes the importance of an LF meal to avoid transient positive fat imbalance.     

Increased Carbohydrate Induced Ghrelin Secretion in Obese vs. Normal‐weight Adolescent Girls

Orexigenic and anorexigenic pathways mediate food intake and may be affected by meal composition. Our objective was to determine whether changes in levels of active ghrelin and peptide YY (PYY) differ in obese vs. normal‐weight adolescent girls following specific macronutrient intake and predict hunger and subsequent food intake. We enrolled 26 subjects: 13 obese and 13 normal‐weight girls, 12–18 years old, matched for maturity (as assessed by bone age) and race. Subjects were assigned a high‐carbohydrate, high‐protein, and high‐fat breakfast in random order. Active ghrelin and PYY were assessed for 4 h after breakfast and 1 h after intake of a standardized lunch. Hunger was assessed using a standardized visual analog scale (VAS). No suppression in active ghrelin levels was noted following macronutrient intake in obese or normal‐weight girls. Contrary to expectations, active ghrelin increased in obese girls following the high‐carbohydrate breakfast, and the percent increase was higher than in controls (P = 0.046). Subsequent food intake at lunch was also higher (P = 0.03). Following the high‐fat breakfast, but not other breakfasts, percent increase in PYY was lower (P = 0.01) and subsequent lunch intake higher (P = 0.005) in obese compared with normal‐weight girls. In obese adolescents, specific intake of high‐carbohydrate and high‐fat breakfasts is associated with greater increases in ghrelin, lesser increases in PYY, and higher intake at a subsequent meal than in controls. Changes in anorexigenic and orexigenic hormones in obese vs. normal‐weight adolescents following high‐carbohydrate and high‐fat meals may influence hunger and satiety signals and subsequent food intake.     

Genetic Effects on Postprandial Variations of Inflammatory Markers in Healthy Individuals

Circulating levels of inflammatory markers predict the risk of cardiovascular disease (CVD), mediated perhaps in part by dietary fat intake, through mechanisms only partially understood. To evaluate post‐fat load changes in inflammatory markers and genetic influences on these changes, we administered a standardized high‐fat meal to 838 related Amish subjects as part of the Heredity and Phenotype Intervention (HAPI) Heart Study and measured a panel of inflammatory markers, including C‐reactive protein (CRP), interleukin‐1β (IL‐1β), matrix metalloproteinase‐1 and ‐9 (MMP‐1 and MMP‐9), and white blood cell (WBC) count, before and 4 h after fat challenge (CRP prechallenge only). Heritabilities (h² ± s.d.) of basal inflammatory levels ranged from 16 ± 8% for MMP‐9 (P = 0.02) to 90 ± 7% for MMP‐1 (P < 0.0001). Post‐fat load, circulating levels of WBC, MMP‐1, and MMP‐9 increased by 16, 32, and 43% (all P < 0.0001), with no significant changes in IL‐1β. Postprandial changes over the 4‐h period were modestly heritable for WBC (age‐ and sex‐adjusted h² = 14 ± 9%, P = 0.04), but the larger MMP‐1 and MMP‐9 changes appeared to be independent of additive genetic effects. These results reveal that a high‐fat meal induces a considerable inflammatory response. Genetic factors appear to play a significant role influencing basal inflammatory levels but to have minimal influence on post‐fat intake inflammatory changes.     

Energy‐Restricted High‐Fat Diets Only Partially Improve Markers of Systemic and Adipose Tissue Inflammation

This study aimed at investigating whether the weight loss due to energy‐restricted high‐fat diets is accompanied with parallel improvements in metabolic markers and adipose tissue inflammation. Eight‐week‐old C57BL/6J mice were given free access to a low‐fat (LF) or a high‐fat (45% of energy from fat—HF) diet for 6 months. Restricting intake of the HF diet by 30% (HFR) during the last 2 months of the HF feeding trial decreased fasting plasma insulin, homeostasis model assessment of insulin resistance (HOMA_IR), and plasma triglyceride levels and improved hepatic steatosis compared to ad libitum HF feeding, indicating an improved metabolic profile. Further, analysis of gonadal white adipose tissue (GWAT) gene expression by microarray and quantitative PCR analyses demonstrated that HFR downregulated expression of genes linked to cell and focal adhesion, cytokine‐cytokine receptor interaction, and endoplasmic reticulum (ER)–associated degradation pathway. However, HFR had no effect on circulating plasminogen activator inhibitor‐1 (PAI‐1) and nonesterified fatty acid levels, which were persistently higher in both HF and HFR groups compared to the LF group. Furthermore, HFR had a negative effect on plasma total adiponectin level. Finally, while HFR decreased GWAT monocyte chemotactic protein‐1 (MCP‐1), interleukin‐2 (IL‐2), and PAI‐1 levels, it did not affect several other cytokines including granulocyte‐macrophage colony‐stimulating factor, interferon‐γ, IL‐1β, IL‐6, and IL‐10. In summary, energy‐restricted high‐fat diets improve insulin sensitivity, while only partially improving markers of systemic and adipose tissue inflammation. In conclusion, our study supports the recommended low‐fat intake for overall cardiovascular health.     

Peptide‐YY Levels after a Fat Load in Black and White Women

Objective: To determine whether basal plasma peptide‐YY (PYY) levels in overweight, middle‐aged black women are different from those of white women of similar BMI and age and ascertain whether there is a difference between the two groups in plasma PYY levels in response to a liquid high fat load. Research Methods and Procedures: Using a commercial radioimmunoassay kit, the concentration of PYY was measured at baseline and at 2, 4, 6, and 8 hours after ingesting a fatty liquid meal (86.5% of the calories from fat) in 12 black and 12 white women who were matched for age and BMI. Results: PYY levels (picograms per milliliter) at baseline and at every other time‐point of the test meal were significantly lower in the black than in the white group. In addition, the change in PYY concentration from baseline was lower in the black than in the white group only at 8 hours after the meal. Discussion: The lower baseline level and the blunted PYY response of the black women to the fat load indicated that this signal for appetite suppression was reduced, which, in turn, might contribute to the enhanced obesity of the black women.     

PPARγ Expression After a High‐fat Meal Is Associated With Plasma Superoxide Dismutase Activity in Morbidly Obese Persons

Peroxisome proliferator‐activated receptor‐γ (PPARγ) may play a protective role in the regulation of vascular function, partly mediated by its effects on superoxide dismutase (SOD). The aim of this study was to determine the association between PPARγ expression in peripheral blood mononuclear cells (PBMCs) and SOD activity in morbidly obese persons with varying degrees of insulin resistance (IR). We studied in 10 morbidly obese persons (five with no IR and five with high IR) the effect of a high‐fat meal on the plasma activity of various antioxidant enzymes and the mRNA expression of PPARγ in PBMC. The high‐fat meal resulted in a significant decrease in plasma SOD activity, glutathione reductase (GSH‐Rd) activity, and mRNA expression of PPARγ only in the group of morbidly obese persons with high IR. PPARγ expression after the high‐fat meal correlated with the IR levels (r = ?0.803, P = 0.009) and the plasma SOD activity (r = 0.903, P = 0.001). Likewise, the reduction in PPARγ expression correlated with the increase in free fatty acids (FFA) (r = 0.733, P = 0.016). In conclusion, the decreased expression of PPARγ in PBMC in morbidly obese persons after a high‐fat meal was associated with the state of IR, the plasma SOD activity, and the changes in the concentration of FFA.     

Meal Pattern Analysis of Diet‐Induced Obesity in Susceptible and Resistant Rats

Objective: To characterize the meal patterns of free feeding Sprague‐Dawley rats that become obese or resist obesity when chronically fed a high‐fat diet. Research Methods and Procedures: Male Sprague‐Dawley rats (N = 120) were weaned onto a high‐fat diet, and body weight was monitored for 19 weeks. Rats from the upper [diet‐induced obese (DIO)] and lower [diet‐resistant (DR)] deciles for body‐weight gain were selected for study. A cohort of chow‐fed (CF) rats weight‐matched to the DR group was also studied. Food intake was continuously monitored for 7 consecutive days using a BioDAQ food intake monitoring system. Results: DIO rats were obese, hyperphagic, hyperleptinemic, hyperinsulinemic, hyperglycemic, and hypertriglyceridemic relative to the DR and CF rats. The hyperphagia of DIOs was caused by an increase in meal size, not number. CF rats ate more calories than DR rats; however, this was because of an increase in meal number, not size. When expressed as a function of lean mass, CF and DR rats consumed the same amount of calories. The intermeal intervals of DIO and DR rats were similar; both were longer than CF rats. The nocturnal satiety ratio of DIO rats was significantly lower than DR and CF rats. The proportion of calories eaten during the nocturnal period did not differ among groups. Discussion: The hyperphagia of a Sprague‐Dawley rat model of chronic diet‐induced obesity is caused by an increase in meal size, not number. These results are an important step toward understanding the mechanisms underlying differences in feeding behavior of DIO and DR rats.     

Altered Hypothalamic Signaling and Responses to Food Deprivation in Rats Fed a Low‐Carbohydrate Diet

Objective: To model how consuming a low‐carbohydrate (LC) diet influences food intake and body weight. Research Methods and Procedures: Food intake and body weight were monitored in rats with access to chow (CH), LC‐high‐fat (HF), or HF diets. After 8 weeks, rats received intracerebroventricular injections of a melanocortin agonist (melanotan‐II) and antagonist (SHU9119), and feeding responses were measured. At sacrifice, plasma hormones and hypothalamic expression of mRNA for proopiomelanocortin (POMC), melanocortin‐4 receptor, neuropeptide Y (NPY), and agouti related protein (AgRP) were assessed. A second set of rats had access to diet (chow or LC‐HF) for 4 weeks followed by 24 h food deprivation on two occasions, after which food intake and hypothalamic POMC, NPY, and AgRP mRNA expression were measured. Results: HF rats consumed more food and gained more weight than rats on CH or LC‐HF diets. Despite similar intakes and weight gains, LC‐HF rats had increased adiposity relative to CH rats. LC‐HF rats were more sensitive to melanotan‐II and less sensitive to SHU9119. LC‐HF rats had increased plasma leptin and ghrelin levels and decreased insulin levels, and patterns of NPY and POMC mRNA expression were consistent with those of food‐deprived rats. LC‐HF rats did not show rebound hyperphagia after food deprivation, and levels NPY, POMC, and AgRP mRNA expression were not affected by deprivation. Discussion: Our results demonstrate that an LC diet influences multiple systems involved in the controls of food intake and body weight. These data also suggest that maintenance on an LC‐HF diet affects food intake by reducing compensatory responses to food deprivation.     

Excessive Energy Intake Does Not Modify Fed‐state Tissue Protein Synthesis Rates in Adult Rats

The impact of chronic excessive energy intake on protein metabolism is still controversial. Male Wistar rats were fed ad libitum during 5 weeks with either a high‐fat high‐sucrose diet (HF: n = 9) containing 45% of total energy as lipids (protein 14%; carbohydrate 40% with 83.5% sucrose) or a standard diet (controls: n = 10). Energy intake and body weight were recorded. At the end of the experiment, we measured body composition, metabolic parameters (plasma amino acid, lipid, insulin, and glucose levels), inflammatory parameter (plasma α2‐macroglobulin), oxidative stress parameters (antioxidant enzyme activities, lipoperoxidation (LPO), protein carbonyl content in liver and muscle), and in vivo fed–state fractional protein synthesis rates (FSRs) in muscle and liver. Energy intake was significantly higher in HF compared with control rats (+28%). There were significant increases in body weight (+8%), body fat (+21%), renal (+41%), and epidydimal (+28%) fat pads in HF compared with control rats. No effect was observed in other tissue weights (liver, muscle, spleen, kidneys, intestine). Liver and muscle FSRs, plasma levels of lipids, glucose, insulin and α2‐macroglobulin, soleus and liver glutathione reductase and peroxidase acitivities, MnSOD activity, LPO, and protein carbonyl content were not altered by the HF diet. Only soleus muscle and liver Cu/ZnSOD activity and soleus muscle catalase activities were reduced in HF rats compared with control rats. Thus, chronic excessive energy intake and increased adiposity, in the absence of other metabolic alterations, do not stimulate fed‐state tissue protein synthesis rates.     

Diurnal Changes in Blood Metabolites and Their Relation to Plasma Growth Hormone and Time of Feeding in Mithun Heifers (Bos frontalis)

The aim of the present study was to investigate what, if any, diurnal changes occur in blood metabolites in relation to plasma growth hormone (GH) and feeding time among mithun (Bos frontalis), a semi‐wild ruminant. Blood samples were collected at hourly intervals during a 24 h span from 6 mithun heifers (averaging 2.5 yr of age and averaging 230 kg in weight) that were fed twice a day at 11:00 and 16:00 h. Samples were assayed for plasma GH and blood metabolites, non‐esterified fatty acids (NEFA), glucose, and alpha‐amino nitrogen. The total sampling period was divided into a 1) postprandial (after meal) period (period I: 11:00 to 21:00 h) and 2) interprandial period (period II: 22:00 to 10:00 h) and also into night (20:00 to 05:00 h) and day (06:00 to 10:00 h) periods for statistical analysis. Plasma glucose and alpha‐amino nitrogen levels increased (p<0.01), and plasma NEFA and GH decreased (p<0.01) after each meal. No diurnal rhythmicity was detected in plasma glucose or alpha‐amino nitrogen levels. Interestingly, plasma NEFA and GH levels were higher (p<0.01) during the interprandial (period II) and night periods, indicating an energy deficit that occurred progressively during the interprandial period of nocturnal feed deprivation. In twice‐daily‐fed mithuns we conclude that: 1) plasma metabolites and GH exhibited a definite pattern of change with time of feeding; 2) concentrations of plasma NEFA were higher nocturnally due to an energy deficit and that GH levels were higher during the interprandial period after the second meal; 3) the interprandial period after the second feeding may be considered to constitute a short‐term food deprivation; 4) the longer interprandial period of 19 h in this study between the second and subsequent morning meal may be changed into equally divided feedings to minimize the short‐term energy deficit; and 5) blood sampling for blood metabolites in mithuns should be conducted at a fixed time of day with special emphasis on time of feeding.     

Role of Intraduodenally Administered Enterostatin in Rats: Inhibition of Food

Central and peripheral administration of enterostatin have been reported to reduce fat or high-fat food intake in rats. Enterostatin is formed in the intestinal lumen by tryptic cleavage of pancreatic procolipase during intraluminal fat digestion. The present experiments were designed to test if enterostatin following intraintestinal infusion would affect food intake in a similar way as intracerebraventricularly or intravenously administered enterostatin. Female Sprague-Dawley rats were fitted with a duodenal catheter and adapted to a feeding schedule for 6 hours each day. After 10 days enterostatin (5.65 and 11.3 nmol/kg/min) or saline were infused into the duodenum and food intake measured. Enterostatin significantly reduced high-fat food intake during the 6 hours of feeding, but had no inhibitory effect on low-fat food intake. Addition of tetracaine to the enterostatin infusates blocked the satiating potency of intestinal enterostatin. These results support the hypothesis of a preabsorptive site of action for enterostatin.     

Meal pattern of male rats maintained on histidine-, leucine-, or tyrosine-supplemented diet

Objective: Food intake is known to be affected by macronutrient composition of the diet, and protein manipulation has been reported to alter food intake, but the effect of individual amino acids on eating behavior has not been fully studied. This study investigated the effect of diet supplementation with three individual amino acids on meal pattern in male rats. Research Methods and Procedures: Thirty‐two Sprague‐Dawley rats were randomly divided into four equal groups and fed control diet or histidine (5%)‐, leucine (5%)‐, or tyrosine (5%)‐supplemented diet for 2 weeks and were monitored for their meal pattern. Results: Total food intake and feeding rate of the different groups were not affected, although other components of meal pattern were altered. Histidine supplementation reduced diurnal meal size by 42% (p < 0.05), whereas that of leucine increased nocturnal meal size by ～35% (p < 0.05). Tyrosine supplementation increased food intake of the nocturnal period and decreased that of the diurnal period. Both histidine and tyrosine supplementation elevated fasting plasma insulin levels and suppressed fasting glucose significantly. Discussion: Individual amino acids were found to alter meal pattern differently. Further investigations are required to dissect the involvement of central and peripheral factors in these alterations.     

Effects of a Longitudinal Training Program on Responses to Exercise in Overweight Men

Objective: The aim of this study was to determine how training modifies metabolic responses and lipid oxidation in overweight young male subjects. Research Methods and Procedures: Eleven overweight subjects were selected for a 4‐month endurance training program. Before and after the training period, they cycled for 60 minutes at 50% of their Vo ₂max after an overnight fast or 3 hours after eating a standardized meal. Various metabolic and endocrine parameters, and respiratory exchange ratio values were evaluated. Results: Exercise‐induced plasma norepinephrine concentration increases were similar before and after training in fasted or fed conditions. After food intake, exercise promoted a decrease in plasma glucose and a higher increase in epinephrine than in fasting conditions. The increase in epinephrine after the meal was more marked after training (264 ± 32 vs. 195 ± 35 pg/mL). Training lowered the resting plasma nonesterified fatty acids. During exercise, changes in glycerol were similar to those found before training. Lipid oxidation during exercise was higher in fasting than in fed conditions (15.5 ± 1.4 vs. 22.3 ± 1.7 g/h). Training did not significantly increase fat oxidation when exercise was performed in fed conditions, but it did in fasting conditions (18.6 ± 1.4 vs. 27.2 ± 1.8 g/h). Discussion: Endurance training decreased plasma nonesterified fatty acids, cholesterol, and insulin concentrations. Training increased lipid oxidation during exercise, in fasting conditions, and not when exercise was performed after the meal. During exercise in overweight subjects, the fasting condition seems more suited to oxidizing fat and maintaining glucose homeostasis than a 3‐hour wait after a standard meal.     

Vagal-Central Nervous System Interactions Modulate the Feeding Response to Peripheral Enterostatin

Enterostatin selectively inhibits the intake of dietary fat after both peripheral and central administration. We have investigated the role of the hepatic vagus nerve in modulating the peripheral response to enterostatin in Sprague-Dawley rats adapted to a high fat (HF) diet. Intraperitoneal (ip) enterostatin reduced intake of HF diet after overnight starvation. This response was abolished by selective vagal hepatic branch transection. Immunohistochemical techniques were used to identify the location of Fos protein in brain nuclei after ip enterostatin. Fos protein was evident in the nucleus tractus solitarius (NTS), parabrachial, paraventricular and supraoptic nuclei. The pattern of expression of Fos-like immunoreactivity differed from that induced by the lipoprivic agent β-mercaptoacetate. Transection of the hepatic vagus blocked the central Fos responses to ip enterostatin. We conclude that afferent hepatic vagal nerve activity is required for the feeding response to peripheral enterostatin.     

Insinuation of exacerbated oxidative stress in sucrose-fed rats with a low dietary intake of magnesium: evidence of oxidative damage to proteins

High sucrose diets and low magnesium intake have been independently implicated in induction of oxidative stress in animal models. The aim of this study was to investigate whether low dietary magnesium intake exacerbates the prooxidant effects of high sucrose feeding. Rats were fed control (C), high sucrose (HS); low magnesium (LM) and high sucrose low magnesium (HSLM) diets for 90 days and oxidative stress evaluated in terms of formation of TBARS, advanced oxidation protein products and protein carbonyls. HS and LM rats showed evidence of lipid peroxidation and protein oxidation in plasma and liver. Enhanced oxidative injury to lipids and proteins after HSLM feeding was indicated by increased carbonyl content (p <0.01) and significantly (p <0.005) higher levels of TBARS in plasma and hepatic tissue relative to both HS and LM groups. Altogether, these results illustrate the potential detrimental and cumulative effects of low magnesium intake combined with high sucrose consumption on oxidative stress variables.