Weight regain after sustained weight reduction is accompanied by suppressed oxidation of dietary fat and adipocyte hyperplasia

2008 ◽  
Vol 294 (4) ◽  
pp. R1117-R1129 ◽  
Author(s):  
Matthew R. Jackman ◽  
Amy Steig ◽  
Janine A. Higgins ◽  
Ginger C. Johnson ◽  
Brooke K. Fleming-Elder ◽  
...  
Keyword(s):  
Dietary Fat ◽  
Weight Regain ◽  
Fat Oxidation ◽  
Free Access ◽  
Low Fat ◽  
Low Fat Diet ◽  
Reduced Body ◽  
Obese Rats ◽  
Male Wistar Rats ◽  
A Minor

A dual-tracer approach (dietary 14C-palmitate and intraperitoneal 3H-H2O) was used to assess the trafficking of dietary fat and net retention of carbon in triglyceride depots during the first 24 h of weight regain. Obesity-prone male Wistar rats were allowed to mature under obesogenic conditions for 16 wk. One group was switched to ad libitum feeding of a low-fat diet for 10 wk (Obese group). The remaining rats were switched to an energy-restricted, low-fat diet for 10 wk that reduced body weight by 14% and were then assessed in energy balance (Reduced group), with free access to the low-fat diet (Relapse-Day1 group), or with a provision that induced a minor imbalance (+10 kcal) equivalent to that observed in obese rats (Gap-Matched group). Fat oxidation remained at a high, steady rate throughout the day in Obese rats, but was suppressed in Reduced, Gap-Matched, and Relapse-Day1 rats though 9, 18, and 24 h, respectively. The same caloric excess in Obese and Gap-Matched rats led to less fat oxidation over the day and greater trafficking of dietary fat to visceral depots in the latter. In addition to trafficking nutrients to storage, Relapse-Day1 rats had more small, presumably new, adipocytes at the end of 24 h. Dietary fat oxidation at 24 h was related to the phosphorylation of skeletal muscle acetyl-CoA carboxylase and fatty acid availability. These observations provide evidence of adaptations in the oxidation and trafficking of dietary fat that extend beyond the energy imbalance, which facilitate rapid, efficient regain during the relapse to obesity.

scholarly journals The effect of pre-resection obesity on post-resection body composition after 75% small bowel resection in rats

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Neesha S. Patel ◽  
Ujwal R. Yanala ◽  
Shruthishree Aravind ◽  
Roger D. Reidelberger ◽  
Jon S. Thompson ◽  
...  
Keyword(s):  
Body Weight ◽  
Small Bowel ◽  
Lean Mass ◽  
Bowel Resection ◽  
Small Bowel Resection ◽  
High Fat ◽  
Low Fat ◽  
Low Fat Diet ◽  
Massive Resection ◽  
Obese Rats

AbstractIn patients with short bowel syndrome, an elevated pre-resection Body Mass Index may be protective of post-resection body composition. We hypothesized that rats with diet-induced obesity would lose less lean body mass after undergoing massive small bowel resection compared to non-obese rats. Rats (CD IGS; age = 2 mo; N = 80) were randomly assigned to either a high-fat (obese rats) or a low-fat diet (non-obese rats), and fed ad lib for six months. Each diet group then was randomized to either underwent a 75% distal small bowel resection (massive resection) or small bowel transection with re-anastomosis (sham resection). All rats then were fed ad lib with an intermediate-fat diet (25% of total calories) for two months. Body weight and quantitative magnetic resonance-determined body composition were monitored. Preoperative body weight was 884 ± 95 versus 741 ± 75 g, and preoperative percent body fat was 35.8 ± 3.9 versus 24.9 ± 4.6%; high-fat vs. low fat diet, respectively (p < 0.0001); preoperative diet type had no effect on lean mass. Regarding total body weight, massive resection produced an 18% versus 5% decrease in high-fat versus low-fat rats respectively, while sham resection produced a 2% decrease vs. a 7% increase, respectively (p < 0.0001, preoperative vs. necropsy data). Sham resection had no effect on lean mass; after massive resection, both high-fat and low-fat rats lost lean mass, but these changes were not different between the latter two rat groups. The high-fat diet and low-fat diet induced obesity and marginal obesity, respectively. The massive resection produced greater weight loss in high-fat rats compared to low-fat rats. The type of dietary preconditioning had no effect on lean mass loss after massive resection. A protective effect of pre-existing obesity on lean mass after massive intestinal resection was not demonstrated.

Metabolic adjustments with the development, treatment, and recurrence of obesity in obesity-prone rats

2004 ◽  
Vol 287 (2) ◽  
pp. R288-R297 ◽  
Author(s):  
Paul S. MacLean ◽  
Janine A. Higgins ◽  
Ginger C. Johnson ◽  
Brooke K. Fleming-Elder ◽  
John C. Peters ◽  
...  
Keyword(s):  
Weight Loss ◽  
Weight Regain ◽  
Weight Maintenance ◽  
Fat Free Mass ◽  
Free Access ◽  
Metabolic Efficiency ◽  
Carbohydrate Utilization ◽  
Reduced Body ◽  
Ad Libitum Feeding ◽  
Urinary Nitrogen

Obesity is reaching epidemic proportions and predisposes afflicted individuals to several comorbidities. For these individuals, losing weight has proven to be an easier feat than maintaining a reduced weight. In obesity-prone rats, we examined if there is a metabolic propensity to regain weight after a period of significant weight loss. Twenty-four-hour energy expenditure (EE), sleeping metabolic rate (SMR), and nonprotein respiratory quotient (NPRQ) were obtained by indirect calorimetry with urinary nitrogen analysis and normalized to fat mass (FM) and fat-free mass (FFM) acquired by dual-energy X-ray absorptiometry. Obesity-prone rats were examined after free access to a high-fat diet for 16 wk to establish the obese state. They were again examined after 2 wk of calorie restriction, which reduced body weight (14%) and FM (32%). Rats were again examined after a further 8 wk of intake-regulated weight maintenance or ad libitum feeding that led to weight regain. Metabolic data were compared with preobese and age-matched controls. Weight loss suppressed EE and SMR beyond what was expected for the change in metabolic mass. This elevated metabolic efficiency persisted throughout weight maintenance but resolved after 8 wk of regain. Adjusted NPRQ values were elevated in weight-maintained and weight-regaining rats, suggesting a preference for carbohydrate utilization. These data support the concept that weight reduction in obesity is accompanied by metabolic adjustments beyond the drive to consume calories that predispose to weight regain, and some aspects of this adjustment persist with prolonged weight maintenance and during weight regain.

Cafeteria diet-induced insulin resistance is not associated with decreased insulin signaling or AMPK activity and is alleviated by physical training in rats

2010 ◽  
Vol 299 (2) ◽  
pp. E215-E224 ◽  
Author(s):  
Nina Brandt ◽  
Katrien De Bock ◽  
Erik A. Richter ◽  
Peter Hespel
Keyword(s):  
Insulin Resistance ◽  
Exercise Training ◽  
Energy Intake ◽  
Insulin Signaling ◽  
Molecular Mechanisms ◽  
Cafeteria Diet ◽  
Low Fat ◽  
Low Fat Diet ◽  
Male Wistar Rats ◽  
Syntaxin 4

Excess energy intake via a palatable low-fat diet (cafeteria diet) is known to induce obesity and glucose intolerance in rats. However, the molecular mechanisms behind this adaptation are not known, and it is also not known whether exercise training can reverse it. Male Wistar rats were assigned to 12-wk intervention groups: chow-fed controls (CON), cafeteria diet (CAF), and cafeteria diet plus swimming exercise during the last 4 wk (CAFTR). CAF feeding led to increased body weight (16%, P < 0.01) and increased plasma glucose ( P < 0.05) and insulin levels ( P < 0.01) during an IVGTT, which was counteracted by training. In the perfused hindlimb, insulin-stimulated glucose transport in red gastrocnemius muscle was completely abolished in CAF and rescued by exercise training. Apart from a tendency toward an ∼20% reduction in both basal and insulin-stimulated Akt Ser473 phosphorylation ( P = 0.051) in the CAF group, there were no differences in insulin signaling (IR Tyr1150/1151, PI 3-kinase activity, Akt Thr308, TBC1D4 Thr642, GSK3-α/β Ser21/9) or changes in AMPKα1 or -α2, GLUT4, Munc18c, or syntaxin 4 protein expression or in phosphorylation of AMPK Thr172 among the groups. In conclusion, surplus energy intake of a palatable but low-fat cafeteria diet resulted in obesity and insulin resistance that was rescued by exercise training. Interestingly, insulin resistance was not accompanied by major defects in the insulin-signaling cascade or in altered AMPK expression or phosphorylation. Thus, compared with previous studies of high-fat feeding, where insulin signaling is significantly impaired, the mechanism by which CAF diet induces insulin resistance seems different.

Acute changes in the response to peripheral leptin with alteration in the diet composition

2001 ◽  
Vol 280 (2) ◽  
pp. R504-R509 ◽  
Author(s):  
L. Lin ◽  
R. Martin ◽  
A. O. Schaffhauser ◽  
D. A. York
Keyword(s):  
Food Intake ◽  
Dietary Fat ◽  
High Fat Diet ◽  
Corticosterone Level ◽  
Inhibitory Response ◽  
Leptin Resistance ◽  
High Fat ◽  
Low Fat ◽  
Low Fat Diet ◽  
Alternative Diet

Dietary induced obesity in rodents is associated with a resistance to leptin. We have investigated the hypothesis that dietary fat per se alters the feeding response to peripheral leptin in rats that were fed either their habitual high- or low-fat diet or were naively exposed to the alternative diet. Osborne-Mendel rats were adapted to either high- or low-fat diet. Food-deprived rats were given either leptin (0.5 mg/kg body wt ip) or saline, after which they were provided with either their familiar diet or the alternative diet. Food intake of rats adapted and tested with the low-fat diet was reduced 4 h after leptin injection, whereas rats adapted and tested with a high-fat diet did not respond to leptin. Leptin was injected again 1 and 5 days after the high-fat diet-adapted rats were switched to the low-fat diet. Leptin reduced the food intake on both days. In contrast, when low-fat diet-adapted rats were switched to a high-fat diet, the leptin inhibitory response was present on day 1 but not observed on day 5. Peripheral injection of leptin increased serum corticosterone level and decreased hypothalamic neuropeptide Y mRNA expression in rats fed the low-fat but not the high-fat diet for 20 days. The data suggest that dietary fat itself, rather than obesity, may induce leptin resistance within a short time of exposure to a high-fat diet.

THE EFFECT OF RAPESEED OIL ON REPRODUCTION AND ON THE COMPOSITION OF RAT MILK FAT

1961 ◽  
Vol 39 (2) ◽  
pp. 195-201 ◽  
Author(s):  
Joyce L. Beare ◽  
E. R. W. Gregory ◽  
D. Morison Smith ◽  
J. A. Campbell
Keyword(s):  
Fatty Acids ◽  
Oleic Acid ◽  
Olive Oil ◽  
Dietary Fat ◽  
Milk Fat ◽  
Rapeseed Oil ◽  
Corn Oil ◽  
Saturated Fatty Acids ◽  
Low Fat ◽  
Low Fat Diet

Rats fed corn oil or a mixture of lard and olive oil produced as many offspring as those receiving no fat supplement with a low-fat commercial meal, but the weanling weight was lower. Although rats fed rapeseed oil continued to reproduce they had fewer and smaller offspring than rats fed other diets.The composition of fatty acids in the milk varied with the dietary fat of the mother. Animals receiving the low-fat diet secreted predominantly saturated fatty acids. A high proportion of linoleic acid appeared in the milk when corn oil was fed, and of oleic acid when the mixture of lard and olive oil was fed. Eicosenoic and erucic acids were present in the milk of rats receiving rapeseed oil, but were less prevalent than in the original oil.

scholarly journals Effect of a long-term high-protein diet on survival, obesity development, and gut microbiota in mice

2016 ◽  
Vol 310 (11) ◽  
pp. E886-E899 ◽  
Author(s):  
Pia Kiilerich ◽  
Lene Secher Myrmel ◽  
Even Fjære ◽  
Qin Hao ◽  
Floor Hugenholtz ◽  
...  
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
Gut Microbiota ◽  
Dietary Fat ◽  
High Fat Diet ◽  
High Fat ◽  
Low Fat ◽  
Low Fat Diet ◽  
Low Protein

Female C57BL/6J mice were fed a regular low-fat diet or high-fat diets combined with either high or low protein-to-sucrose ratios during their entire lifespan to examine the long-term effects on obesity development, gut microbiota, and survival. Intake of a high-fat diet with a low protein/sucrose ratio precipitated obesity and reduced survival relative to mice fed a low-fat diet. By contrast, intake of a high-fat diet with a high protein/sucrose ratio attenuated lifelong weight gain and adipose tissue expansion, and survival was not significantly altered relative to low-fat-fed mice. Our findings support the notion that reduced survival in response to high-fat/high-sucrose feeding is linked to obesity development. Digital gene expression analyses, further validated by qPCR, demonstrated that the protein/sucrose ratio modulated global gene expression over time in liver and adipose tissue, affecting pathways related to metabolism and inflammation. Analysis of fecal bacterial DNA using the Mouse Intestinal Tract Chip revealed significant changes in the composition of the gut microbiota in relation to host age and dietary fat content, but not the protein/sucrose ratio. Accordingly, dietary fat rather than the protein/sucrose ratio or adiposity is a major driver shaping the gut microbiota, whereas the effect of a high-fat diet on survival is dependent on the protein/sucrose ratio.

The Effect of Long-Term High Protein, Low Carbohydrate, and Low Fat Diet in CKMB Enzymes and Troponin T in Male Wistar Rats

2021 ◽  
Vol 3 (2) ◽  
pp. 58-64
Author(s):  
Asma Amaliah Idrus ◽  
Aryadi Arsyad ◽  
Aminuddin
Keyword(s):  
Wistar Rats ◽  
Troponin T ◽  
High Protein ◽  
Low Fat ◽  
Post Intervention ◽  
Feed Composition ◽  
Low Fat Diet ◽  
Low Carbohydrate ◽  
Male Wistar Rats

Obesity is one of the diseases caused by unhealthy eating patterns and diets. An unhealthy diet can increase cholesterol levels in the blood which will then accumulate on the inner walls of blood vessels, causing atherosclerosis. This study aims to determine the effect of long-term high-protein, low-carbohydrate and low-fat diet on heart function by examining male CKMB & Troponin T levels of Rattus Norvegicus. This research was conducted experimentally in a laboratory with a Post-Test Control Design Group research design. The number of samples was 20 male wistar rats and divided into two groups (standard feed group) and the TPRKRL diet (high protein, low carbohydrate, low fat diet group). Blood was examined in the Hasanuddin University medical research center laboratory using the ELIZA method. The analysis used to determine the difference between the two groups was the Maan-Whitney test. The results showed that the macronutrient composition of the high-protein diet had significantly higher protein content and percentage and lower carbohydrates (protein 78.25% vs. 15.25%; CHO 10.5% vs. 52.2%) compared to the standard feed composition. Meanwhile, post-intervention blood and organ Troponin T levels in the treatment group were 25.45 ± 1.80 and 1022.52 ± 447.89 pg/ml, respectively. And post-intervention blood and organ Troponin T levels in the control group were 23.99 ± 1.24 and 1117.56 ± 324.44 pg/ml. The TPRLLK diet was able to significantly reduce body weight compared to the standard diet and the TPRLLK diet did not increase the enzyme markers of heart damage.

scholarly journals Alterations in mood after changing to a low-fat diet

1998 ◽  
Vol 79 (1) ◽  
pp. 23-30 ◽  
Author(s):  
Anita S. Wells ◽  
Nicholas W. Read ◽  
Jonathan D. E. Laugharne ◽  
N. S. Ahluwalia
Keyword(s):  
Dietary Fat ◽  
Plasma Cholesterol ◽  
Intervention Group ◽  
Hdl Cholesterol ◽  
Diet Group ◽  
Total Serum ◽  
Control Group ◽  
Total Serum Cholesterol ◽  
Low Fat ◽  
Low Fat Diet

The effects on mood of reducing dietary fat while keeping the energy constant were examined in ten male and ten female healthy volunteers aged between 20 and 37 years. Each volunteer consumed a diet containing 41% energy as fat for 1 month. For the second month half of the subjects changed to a low-fat diet (25% energy from fat) and the remainder continued to eat the diet containing 41% energy from fat. Changes in mood and blood lipid concentrations were assessed before, during and at the end of the study. Profile of mood states (POMS) ratings of anger–hostility significantly increased in the intervention group after 1 month on the low-fat diet, while during the same period there was a slight decline in anger–hostility in the control subjects (group F 6.72; df 1,14; P = 0.021). Tension–anxiety ratings declined in the control group consuming the higher fat diet but did not change in the group consuming the low-fat diet (group F 6.34; df 1,14; P = 0.025). There was a decline in fasting concentrations of HDL-cholesterol after the low-fat diet and a small increase in subjects consuming the medium-fat diet (group F 4.96; df 1,12; P = 0.046), but no significant changes in concentrations of total serum cholesterol, LDL-cholesterol or triacylglycerol were observed. The results suggest that a change in dietary fat content from 41 to 25% energy may have adverse effects on mood. The alterations in mood appear to be unrelated to changes in fasting plasma cholesterol concentrations.

scholarly journals The role of dietary fat in obesity-induced insulin resistance

2016 ◽  
Vol 311 (6) ◽  
pp. E989-E997 ◽  
Author(s):  
Denise E. Lackey ◽  
Raul G. Lazaro ◽  
Pingping Li ◽  
Andrew Johnson ◽  
Angelina Hernandez-Carretero ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Dietary Fat ◽  
High Fat Diet ◽  
Caloric Intake ◽  
High Fat ◽  
Low Fat ◽  
Feeding Method ◽  
Low Fat Diet ◽  
Obesity And Diabetes

Consumption of excess calories results in obesity and insulin resistance and has been intensively studied in mice and humans. The objective of this study was to determine the specific contribution of dietary fat rather than total caloric intake to the development of obesity-associated insulin resistance. We used an intragastric feeding method to overfeed excess calories from a low-fat diet (and an isocalorically matched high-fat diet) through a surgically implanted gastric feeding tube to generate obesity in wild-type mice followed by hyperinsulinemic-euglycemic clamp studies to assess the development of insulin resistance. We show that overfeeding a low-fat diet results in levels of obesity similar to high-fat diet feeding in mice. However, despite a similar body weight, obese high-fat diet-fed mice are more insulin resistant than mice fed an isocaloric low-fat diet. Therefore, increased proportion of calories from dietary fat further potentiates insulin resistance in the obese state. Furthermore, crossover diet studies revealed that reduction in dietary fat composition improves glucose tolerance in obesity. In the context of the current obesity and diabetes epidemic, it is particularly important to fully understand the role of dietary macronutrients in the potentiation and amelioration of disease.

scholarly journals High fat meals increases postprandial fat oxidation rate but not postprandial lipemia

2019 ◽  
Vol 18 (1) ◽  
Author(s):  
Chih-Hui Chiu ◽  
Tsung-Jen Yang ◽  
Che-Hsiu Chen ◽  
Ming-Jing Zeng
Keyword(s):  
Oxidation Rate ◽  
Postprandial Lipemia ◽  
Random Order ◽  
Fat Oxidation ◽  
Calorie Intake ◽  
High Fat ◽  
Low Fat ◽  
Low Fat Diet ◽  
Postprandial Triglyceride ◽  
Fat Meal

Abstract Background This study investigated the effects of ingesting meals with the same calorie intake but distinct nutritional contents after exercise on postprandial lipemia the next day. Methods Eight healthy male participants completed two 2-day trials in a random order. On day 1, the participants underwent five 12 min bouts of cycling exercise with a bout of higher intensity exercise (4 min) after each and then a bout of lower intensity cycling (2 min). The total exercise time was 90 min. After the exercise, the participants ingested three high-fat or low-fat meals. On Day 2, the participants were asked to rest in the laboratory and ingest a high-fat meal. Their postprandial reaction after a high-fat meal was observed. Results Postprandial triglyceride concentrations in the high-fat diet trial and low-fat diet trial exhibited nonsignificant differences. Total TG AUC were no significantly different on HF trial and LF trial (HF: 6.63 ± 3.2; LF: 7.20 ± 3.4 mmol/L*4 h. p = 0.586). However, the postprandial fat oxidation rate total AUC (HF: 0.58 ± 0.1; LF: 0.39 ± 0.2 g/min*4 h. p = 0.045), plasma glucose, and insulin concentration of the high-fat trial were significantly higher than those of the low-fat trial. Conclusions This study revealed that meals with distinct nutritional contents after a 90-min exercise increased the postprandial fat oxidation rate but did not influence the postprandial lipemia after a high-fat meal the next day.

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