Leptin responses to glucose infusions in obesity-prone rats

2000 ◽  
Vol 279 (5) ◽  
pp. E1088-E1096 ◽  
Author(s):  
James R. Levy ◽  
John Lesko ◽  
Richard J. Krieg ◽  
Robert A. Adler ◽  
Wayne Stevens
Keyword(s):  
Body Fat ◽  
High Fat Diet ◽  
Leptin Resistance ◽  
Sprague Dawley ◽  
High Fat ◽  
Intravenous Glucose ◽  
Fischer 344 ◽  
Fat Stores ◽  
Diet Control ◽  
Plasma Leptin

The secretion of leptin is dually regulated. In fasting animals, plasma leptin concentrations reflect body fat stores, whereas the incremental leptin response to fasting or refeeding most likely reflects insulin-mediated energy flux and metabolism within adipocytes. Impaired secretion of leptin in either pathway could result in obesity. We therefore measured plasma leptin concentrations in fasted animals and plasma leptin concentrations after an intravenous glucose infusion in a rat model of obesity. Young Sprague-Dawley (S-D) and Fischer 344 (F344) rats had similar percent body fat and fasting glucose and fasting leptin concentrations. However, F344 animals had higher insulin concentrations and leptin responses to intravenous glucose than did the S-D animals. The animals were then fed a control or high-fat diet for 6 wk. High-fat fed animals gained more weight and body fat than did the control fed animals. Control and high-fat fed F344 animals gained ∼40% ( P < 0.0001) more weight and >100% ( P < 0.01) more body fat than did the S-D animals. Fasting leptin concentrations and leptin concentrations after intravenous glucose infusions and feeding were more than double ( P < 0.05) in F344 animals compared with S-D animals. Whether an animal is fed a control or high-fat diet had little effect on the leptin response to intravenous glucose. In conclusion, young, lean F344 animals, before the onset of obesity, demonstrated a greater acute leptin response to intravenous glucose than similarly lean S-D animals. After a 6-wk diet, F344 animals had a greater percent increase in body weight and insulin resistance and exhibited higher fasting leptin concentrations and a greater absolute leptin response to intravenous glucose compared with the S-D animals. The chronic diet (control or high fat) had little impact on the acute leptin response to intravenous glucose. F344 animals exhibit leptin resistance in young, lean animals and after aging and fat accumulation.

High-fat diet is associated with blunted splanchnic sympathoinhibitory responses to gastric leptin and cholecystokinin: implications for circulatory control

2011 ◽  
Vol 300 (3) ◽  
pp. H961-H967 ◽  
Author(s):  
Jackie M. Y. How ◽  
Barbara C. Fam ◽  
Anthony J. M. Verberne ◽  
Daniela M. Sartor
Keyword(s):  
Arterial Pressure ◽  
High Fat Diet ◽  
Cardiovascular Effects ◽  
Vagal Afferents ◽  
Sprague Dawley ◽  
High Fat ◽  
Lower Plasma ◽  
Lower Tertile ◽  
Circulatory Control ◽  
Plasma Leptin

Gastric leptin and cholecystokinin (CCK) act on vagal afferents to induce cardiovascular effects and reflex inhibition of splanchnic sympathetic nerve discharge (SSND) and may act cooperatively in these responses. We sought to determine whether these effects are altered in animals that developed obesity in response to a medium high-fat diet (MHFD). Male Sprague-Dawley rats were placed on a low-fat diet (LFD; n = 8) or a MHFD ( n = 24) for 13 wk, after which the animals were anesthetized and artificially ventilated. Arterial pressure was monitored and blood was collected for the determination of plasma leptin and CCK. SSND responses to leptin (15 μg/kg) and CCK (2 μg/kg) administered close to the coeliac artery were evaluated. Collectively, MHFD animals had significantly higher plasma leptin but lower plasma CCK levels than LFD rats ( P < 0.05), and this corresponded to attenuated or reversed SSND responses to CCK (LFD, −21 ± 2%; and MHFD, −12 ± 2%; P < 0.05) and leptin (LFD, −6 ± 2%; and MHFD, 4 ± 1%; P < 0.001). Alternatively, animals on the MHFD were stratified into obesity-prone (OP; n = 8) or obesity-resistant (OR; n = 8) groups according to their weight gain falling within the upper or lower tertile, respectively. OP rats had significantly higher resting arterial pressure, adiposity, and plasma leptin but lower plasma CCK compared with LFD rats ( P < 0.05). The SSND responses to CCK or leptin were not significantly different between OP and OR animals. These results demonstrate that a high-fat diet is associated with blunted splanchnic sympathoinhibitory responses to gastric leptin and CCK and may impact on sympathetic vasomotor mechanisms involved in circulatory control.

Abstract 15228: Hyperleptinemia Exacerbates High Fat Diet-mediated Atrial Remodeling and Fibrillation

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Yuki Ebata ◽  
Akira Fukui ◽  
Hidekazu Kondo ◽  
Shotaro Saito ◽  
Ichitaro Abe ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Electrophysiological Study ◽  
Leptin Resistance ◽  
Atrial Remodeling ◽  
Conduction Time ◽  
Mrna Levels ◽  
High Fat ◽  
Perfused Heart ◽  
Calmodulin Kinase ◽  
Plasma Leptin

Introduction: Obesity is an independent risk factor of atrial fibrillation (AF). Although serum leptin levels have been reportedly up-regulated in subjects with obesity and metabolic syndrome (leptin resistance), the relation of hyperleptinemia and AF remains to be solved. Hypothesis: We tested the hypothesis whether hyperleptinemia could exacerbate high-fat-diet (HFD)-mediated AF. Methods: Eight-week-old male C57BL/6 (WT) and leptin-deficient ob/ob mice (Ob) were treated either with normal-fat-diet (NFD) or 60% HFD. Eight weeks later, transesophageal burst pacing and electrophysiological study using isolated perfused hearts were performed. The effect of leptin antagonist (LAnt) was also examined using osmotic mini-pump in WT-HFD mice. Results: 1) HFD increased body weight and plasma leptin concentration in WT mice (both p<0.01). 2) Masson trichrome staining revealed that heterogeneous interstitial LA fibrosis was evident in WT-HFD, which was not observed in Ob-HFD (p<0.05). Up-regulation of collagen1, α-SMA, TNF-α, and MCP-1 mRNA levels observed in WT-HFD mice LA, was attenuated in Ob-HFD mice. 3) While transesophageal burst pacing invariably induced AF (8/8, 100%) in WT-HFD mice, it induced AF less frequently (1/8, 12.5%) in Ob-HFD mice (p<0.01). 4) In isolated perfused heart experiments, interatrial conduction time was prolonged in WT-HFD mice, but not in Ob-HFD mice (p<0.05). 5) Western immunoblotting revealed up-regulated expressions of phosphorylated-calmodulin kinase II (p-CamKII) and Na+-Ca2+ exchanger in WT-HFD mice (both p<0.01). However, these changes were attenuated in Ob-HFD mice. 6) LAnt treatment for 4 weeks attenuated the AF inducibility assessed by transesophageal burst pacing (8/8 vs 2/8, p<0.05). Conclusions: Our findings suggest that hyperleptinemia (leptin resistance) plays an essential role in HFD-mediated atrial remodeling and AF. Inhibition of leptin or leptin signaling may become a novel therapeutic target to prevent obesity-related AF.

scholarly journals Jaboticaba (Myrciaria jaboticaba (Vell.) Berg.) peel improved triglycerides excretion and hepatic lipid peroxidation in high-fat-fed rats

2013 ◽  
Vol 26 (5) ◽  
pp. 571-581 ◽  
Author(s):  
Ângela Giovana Batista ◽  
Sabrina Alves Lenquiste ◽  
Carolin Moldenhauer ◽  
Juliana Teixeira Godoy ◽  
Soely Maria Pissini Machado Reis ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
High Fat Diet ◽  
Sprague Dawley ◽  
High Fat ◽  
Hepatic Lipid ◽  
Fecal Lipid ◽  
Freeze Dried ◽  
Triglyceride Content ◽  
Diet Control ◽  
Hepatic Lipid Peroxidation

OBJECTIVE: The aim of this study was to evaluate the influence of high-fat diets with 1%, 2%, and 4% freeze-dried jaboticaba peel on the serum, liver, and fecal lipid profile of obese rats. METHODS: Thirty male Sprague-Dawley rats were divided into 5 groups. Obesity was induced in four groups using a high-fat diet (35% lipids). One group was used as a high-fat diet control (High-fat group - HF). The other three high-fat-diet groups were given 1%, 2%, and 4% freeze-dried jaboticaba peel (High-Fat Jaboticaba - HFJ1, HFJ2, and HFJ4, respectively) in the last 40 experimental days. Blood and the liver were collected after 70 days of treatment and feces were collected in the last experimental week. Total cholesterol, triglycerides, and lipids were measured in the serum, liver, and dried feces. ffer in the experimental groups. HFJ2 group had the highest hepatic and fecal lipid contents compared with the group fed a diet with normal fat content (N), but low hepatic lipid peroxidation. HFJ4 group had the highest mean hepatic and fecal cholesterol levels. Hepatic triglyceride levels did not differ among the groups, and groups HFJ1 and HFJ4 presented the highest fecal triglyceride content. CONCLUSION: The amounts of jaboticaba peel used by this study did not protect against hepatic steatosis or undesired levels of other studied lipids, but it did increase fecal triglycerides. Lipid peroxidation in the liver decreased in the HFJ2 group.

Effect of starvation and food intake on sympathetic activity

1988 ◽  
Vol 255 (2) ◽  
pp. R284-R288 ◽  
Author(s):  
T. Sakaguchi ◽  
K. Arase ◽  
J. S. Fisler ◽  
G. A. Bray
Keyword(s):  
Firing Rate ◽  
High Fat Diet ◽  
Sympathetic Activity ◽  
Nutrient Status ◽  
Nutrient Loads ◽  
Sprague Dawley ◽  
High Fat ◽  
Tissue Mass ◽  
Intravenous Glucose ◽  
Sprague Dawley Rats

These studies have examined the effect of fasting and nutrient loads on sympathetic firing rate in three groups of rats that develop widely divergent degrees of obesity when eating a high-fat diet. Starvation of Sprague-Dawley rats for 24 or 48 h was associated with a decrease in basal sympathetic activity of nearly 25% in the first 24 h and of slightly greater than 30% in 48 h. This decline in sympathetic activity paralleled the loss of body weight and reduction in adipose tissue mass. After starvation for 48 h, Osborne-Mendel rats, which readily develop obesity when eating a high-fat diet, showed a greater decrease in basal sympathetic activity than did the diet-resistant S 5B/P1 rats. A single liquid 36-kcal intragastric meal was associated with an acute 30% increase in sympathetic firing rate in the overnight-fasted Sprague-Dawley rats. The values 3 h after the meal had returned halfway to normal, and by 6 h they were more than 85% of the way to normal. An intravenous injection of glucose produced a greater rise in sympathetic activity in diet-resistant S 5B/P1 rats than in the diet-sensitive Osborne-Mendel rats. These data are consistent with the hypotheses that sympathetic activity is positively related to nutrient status, that it varies between strains of rats, and that it can be acutely increased by an intragastric meal or by intravenous glucose.

Leptin secretion after a high-fat meal in normal-weight rats: strong predictor of long-term body fat accrual on a high-fat diet

2006 ◽  
Vol 290 (2) ◽  
pp. E258-E267 ◽  
Author(s):  
S. F. Leibowitz ◽  
G.-Q. Chang ◽  
J. T. Dourmashkin ◽  
R. Yun ◽  
C. Julien ◽  
...  
Keyword(s):  
Body Fat ◽  
High Fat Diet ◽  
Strong Predictor ◽  
Normal Weight ◽  
Sprague Dawley ◽  
High Fat ◽  
Sprague Dawley Rats ◽  
Orexigenic Peptide ◽  
Fat Meal

The objective of this study was to investigate meal-related endocrine changes that permit one to identify Sprague-Dawley rats at normal weight that are prone (OP) vs. resistant (OR) to obesity. In blood collected via chronic cardiac catheters, a 2-h high-fat meal (HFM, 50% fat, 40 kcal) at dark onset caused a significant increase in leptin, insulin, and triglycerides compared with premeal levels. Similar to patterns in already obese compared with lean rats on a high-fat diet, these meal-induced endocrine changes in normal-weight rats on lab chow were almost twofold larger in OP rats that, compared with OR rats, subsequently accumulated 100% more fat mass on a chronic high-fat diet. These exaggerated endocrine changes were similarly observed in blood collected using a simpler tail vein puncture procedure. In three separate experiments, the HFM-induced rise in leptin was found to be the strongest, positive correlate ( r = +0.58, +0.62 and +0.64) of long-term body fat accrual. The lowest (2–5 ng/ml) vs. highest (6–9 ng/ml) scores for this post-HFM leptin measurement identified distinct OR and OP subgroups, respectively, when they were similar in body weight (340–350 g), premeal leptin (2.6–3.4 ng/ml), and meal size (40 kcal). Subsequent tests in these normal-weight OP rats revealed a distinct characteristic compared with OR rats, namely, exaggerated HFM-induced rise in expression of the orexigenic peptide galanin in the paraventricular nucleus. Thus, with this HFM-induced leptin measurement, OP rats can be identified while still at normal weight and then investigated for mechanisms that contribute to their excessive body fat accrual on a high-fat diet.

scholarly journals Four-Week Consumption of Malaysian Honey Reduces Excess Weight Gain and Improves Obesity-Related Parameters in High Fat Diet Induced Obese Rats

2017 ◽  
Vol 2017 ◽  
pp. 1-9 ◽  
Author(s):  
Suhana Samat ◽  
Francis Kanyan Enchang ◽  
Fuzina Nor Hussein ◽  
Wan Iryani Wan Ismail
Keyword(s):  
Weight Gain ◽  
High Fat Diet ◽  
Physicochemical Analysis ◽  
Excess Weight ◽  
Sprague Dawley ◽  
High Fat ◽  
Excess Weight Gain ◽  
Sprague Dawley Rats ◽  
Acacia Honey ◽  
Plasma Leptin

Many studies revealed the potential of honey consumption in controlling obesity. However, no study has been conducted using Malaysian honey. In this study, we investigated the efficacy of two local Malaysian honey types: Gelam and Acacia honey in reducing excess weight gain and other parameters related to obesity. The quality of both honey types was determined through physicochemical analysis and contents of phenolic and flavonoid. Male Sprague-Dawley rats were induced to become obese using high fat diet (HFD) prior to introduction with/without honey or orlistat for four weeks. Significant reductions in excess weight gain and adiposity index were observed in rats fed with Gelam honey compared to HFD rats. Moreover, levels of plasma glucose, triglycerides, and cholesterol, plasma leptin and resistin, liver enzymes, renal function test, and relative organ weight in Gelam and Acacia honey treated groups were reduced significantly when compared to rats fed with HFD only. Similar results were also displayed in rats treated with orlistat, but with hepatotoxicity effects. In conclusion, consumption of honey can be used to control obesity by regulating lipid metabolism and appears to be more effective than orlistat.

Resistance to Dietary Obesity in Rats Given Different High-Energy Diets

2006 ◽  
Vol 76 (5) ◽  
pp. 271-279 ◽  
Author(s):  
Pérez de Heredia ◽  
Garaulet ◽  
Puy Portillo ◽  
Zamora
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Body Fat ◽  
High Fat Diet ◽  
Wistar Rats ◽  
High Energy ◽  
Sprague Dawley ◽  
High Fat ◽  
Sprague Dawley Rats ◽  
Dietary Obesity

Susceptibility to dietary obesity was studied in Wistar and Sprague-Dawley rats submitted to different high-energy diets. Experiment 1: female Sprague-Dawley rats were fed chow (n = 6) or a high-fat diet (n = 12) for 22 weeks. Experiment 2: Wistar rats were fed chow or a high-fat diet, and Sprague-Dawley rats were given chow, high-fat, sweet condensed milk, or cafeteria diets, for eight weeks (6 animals per group). Food intake and body weight were recorded weekly. Adipose tissue was collected from periovarian, mesenteric, and subcutaneous regions and adipocytes were isolated and measured. Both strains showed similar energy intake and body weight gain. Wistar rats reached greater final body fat contents than Sprague-Dawley rats, regardless of the type of diet. However, resistance to dietary obesity was found in 100% of cases in both experiments. None of the diets succeeded in increasing body fat accumulation when compared to control groups. All adipose tissue locations were equally unaffected, with periovarian fat cells being larger than those in mesenteric and subcutaneous regions in all the groups. In view of the strong resistance to obesity observed in rats, it should be important for researchers to transmit the difficulties of inducing dietary obesity in these animals, in order to prevent bias in science interpretation.

scholarly journals Fructose-induced leptin resistance exacerbates weight gain in response to subsequent high-fat feeding

2008 ◽  
Vol 295 (5) ◽  
pp. R1370-R1375 ◽  
Author(s):  
Alexandra Shapiro ◽  
Wei Mu ◽  
Carlos Roncal ◽  
Kit-Yan Cheng ◽  
Richard J. Johnson ◽  
...  
Keyword(s):  
Weight Gain ◽  
High Fat Diet ◽  
Leptin Resistance ◽  
Sprague Dawley ◽  
High Fat ◽  
Serum Leptin ◽  
Fructose Intake ◽  
Sprague Dawley Rats ◽  
High Fructose ◽  
Subsequent Exposure

It has been suggested that increased fructose intake is associated with obesity. We hypothesized that chronic fructose consumption causes leptin resistance, which subsequently may promote the development of obesity in response to a high-fat diet. Sprague-Dawley rats were fed a fructose-free control or 60% fructose diet for 6 mo and then tested for leptin resistance. Half of the rats in each group were then switched to high-fat diet for 2 wk, while the other half continued on their respective diets. Chronic fructose consumption caused leptin resistance, while serum leptin levels, weight, and adiposity were the same as in control rats that were leptin responsive. Intraperitoneal leptin injections reduced 24-h food intake in the fructose-free group (73.7 ± 6.3 vs. 58.1 ± 8 kcal, P = 0.02) but had no effect in fructose-fed rats (71.2 ± 6.6 vs. 72.4 ± 6.4 kcal, P = 0.9). Absence of anorexic response to intraperitoneal leptin injection was associated with 25.7% decrease in hypothalamic signal transducer and activator of transcription 3 phosphorylation in the high-fructose-fed rats compared with controls ( P = 0.015). Subsequent exposure of the fructose-mediated, leptin-resistant rats to a high-fat diet led to exacerbated weight gain (50.2 ± 2 g) compared with correspondingly fed leptin-responsive animals that were pretreated with the fructose-free diet (30.4 ± 5.8 g, P = 0.012). Our data indicate that chronic fructose consumption induces leptin resistance prior to body weight, adiposity, serum leptin, insulin, or glucose increases, and this fructose-induced leptin resistance accelerates high-fat induced obesity.

Effect of a High-Fat Diet and Occupational Exposure in Different Rat Strains on Lung and Systemic Responses: Examination of the Exposome in an Animal Model

2019 ◽  
Vol 174 (1) ◽  
pp. 100-111 ◽  
Author(s):  
James M Antonini ◽  
Vamsi Kodali ◽  
Mohammad Shoeb ◽  
Michael Kashon ◽  
Katherine A Roach ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Lavage Fluid ◽  
Male Rats ◽  
Brown Norway ◽  
Sprague Dawley ◽  
High Fat ◽  
Health Indices ◽  
Fischer 344 ◽  
Exposed Animal ◽  
Genetic Contributions

Abstract The exposome is the measure of all exposures of an individual in a lifetime and how those exposures relate to health. The goal was to examine an experimental model integrating multiple aspects of the exposome by collecting biological samples during critical life stages of an exposed animal that are applicable to worker populations. Genetic contributions were assessed using strains of male rats with different genetic backgrounds (Fischer-344, Sprague Dawley, and Brown-Norway) maintained on a regular or high-fat diet for 24 weeks. At week 7 during diet maintenance, groups of rats from each strain were exposed to stainless steel welding fume (WF; 20 mg/m3 × 3 h/d × 4 days/week × 5 weeks) or air until week 12, at which time some animals were euthanized. A separate set of rats from each strain were allowed to recover from WF exposure until the end of the 24-week period. Bronchoalveolar lavage fluid and serum were collected at 7, 12, and 24 weeks to assess general health indices. Depending on animal strain, WF exposure and high-fat diet together worsened kidney toxicity as well as altered different serum enzymes and proteins. Diet had minimal interaction with WF exposure for pulmonary toxicity endpoints. Experimental factors of diet, exposure, and strain were all important, depending on the health outcome measured. Exposure had the most significant influence related to pulmonary responses. Strain was the most significant contributor regarding the other health indices examined, indicating that genetic differences possibly drive the exposome effect in each strain.

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