scholarly journals Less is more? Ultra-low carbohydrate diet and working dogs’ performance

PLoS ONE ◽  
2021 ◽  
Vol 16 (12) ◽  
pp. e0261506
Author(s):  
Arnon Gal ◽  
Williams Cuttance ◽  
Nick Cave ◽  
Nicolas Lopez-Villalobos ◽  
Aaron Herndon ◽  
...  

New Zealand farm working dogs are supreme athletes that are crucial to agriculture in the region. The effects that low or high dietary carbohydrate (CHO) content might have on their interstitial glucose (IG) and activity during work are unknown. The goals of the study were to determine if the concentration of IG and delta-g (a measurement of activity) will be lower in dogs fed an ultra-low CHO high fat diet in comparison to dogs fed a high CHO low fat diet, and to determine if low concentrations of IG are followed by reduced physical activity. We hypothesized that feeding working farm dogs an ultra-low CHO diet would reduce their IG concentrations which in turn would reduce physical activity during work. We prospectively recruited 22 farm dogs from four farms. At each farm, dogs were randomized to one of two diets and had a month of dietary acclimation to their allocated diet. The macronutrient proportions as a percentage of metabolizable energy (%ME) for the high CHO low fat diet (Diet 1) were 23% protein, 25% fat, and 52% CHO, and for the ultra-low CHO high fat diet (Diet 2) 37% protein, 63% fat, and 1% CHO. Following the acclimation period, we continuously monitored IG concentrations with flash glucose monitoring devices, and delta-g using triaxial accelerometers for 96 h. Dogs fed Diet 2 had a lower area under the curve (±SE) for IG (AUC Diet 2 = 497 ± 4 mmol/L/96h, AUC Diet 1 = 590 ± 3 mmol/L/96h; P = 0.002) but a higher area under the curve (±SE) for delta-g (AUC Diet 2 = 104,122 ± 6,045 delta-g/96h, AUC Diet 1 = 80,904 ± 4,950 delta-g/96h; P< 0.001). Interstitial glucose concentrations increased as the activity level increased (P < 0.001) and were lower for Diet 2 within each activity level (P < 0.001). The overall incidence of low IG readings (< 3.5 mmol/L) was 119/3810 (3.12%), of which 110 (92.4%) readings occurred in the Diet 2 group (P = 0.001). In the Diet 2 group, 99/110 (90%) of the low IG events occurred during the resting period (19:00–06:00). We conclude that feeding Diet 2 (ultra-low CHO high fat diet) to working farm dogs was associated with increased delta-g despite decreased IG concentrations. Interstitial glucose concentrations were positively associated with dogs’ activity levels independent of diet. Lastly, events of low IG occurred at a low incidence and were predominantly seen between 19:00–06:00 in dogs fed the ultra-low CHO high fat diet.

2009 ◽  
Vol 34 (4) ◽  
pp. 595-602 ◽  
Author(s):  
Constanza Matilde López-Fontana ◽  
Almudena Sánchez-Villegas ◽  
Miguel Angel Martínez-Gonzalez ◽  
José Alfredo Martinez

Inadequate dietary patterns and sedentary lifestyles are believed to be important factors in predisposing people to obesity. This study analyzed the potential interaction between habitual physical activity and the carbohydrate (CHO)-fat distribution in 2 hypocaloric diets and the impact of such interplay on body composition changes. Forty healthy obese women, 20–50 years old, were randomly assigned to a high- or low-CHO energy-restricted diet, which was low or high in fat, respectively, during 10 weeks. Baseline and final measurements were performed to assess dietary habits, resting metabolic rate, and body composition changes. Physical activity was measured with a triaxial accelerometer and with a questionnaire. There were no significant differences in anthropometric and metabolic variables between both dietary groups at baseline. However, there was a positive correlation between total free-living physical activity and arm muscle preservation after 10 weeks (r = 0.371; p = 0.024). Interestingly, an interaction between macronutrient (CHO–fat distribution) intake and physical activity was found, since less-active subjects with a high-CHO–low-fat diet showed a greater fat loss than those more active with a lower-CHO–high-fat diet, whereas more-active subjects with a high-CHO–low-fat diet showed a smaller fat loss than those receiving a low-CHO–high-fat diet. Physical activity and the macronutrient content of energy-restricted diets, when designed to promote body fat mass reduction, should be considered together to better predict the outcome.


2015 ◽  
Vol 35 (suppl_1) ◽  
Author(s):  
Megha Murali ◽  
Carla Taylor ◽  
Peter Zahradka ◽  
Jeffrey Wigle

Background and Objective: Arterial stiffness is recognized as being an independent predictor of incipient vascular disease associated with obesity and metabolic syndrome. In obese subjects, the decrease in the plasma level of adiponectin, an anti-diabetic and anti-atherogenic adipokine, is well known. Hence the aim of our study was to examine the effect of loss of adiponectin on the development of arterial stiffness in response to a high fat diet. Methods and Results: Male 8-week old adiponectin knockout (APN KO) and C57BL/6 (control) mice were fed a high fat diet (60% Calories from fat) for 12 weeks to induce obesity and insulin resistance (n=10/group). APN KO and C57BL/6 mice were fed a low fat diet (10% Calories from fat) and used as lean controls (n=10/group). After 12 weeks on the high fat diet, the APN KO mice weighed significantly more than the C57BL/6 mice (45.1±1.3 g vs 40.1±1.1 g, p=0.0008) but there was no difference in the final weights between genotypes fed the low fat diet. APN KO mice on both high and low fat diets for 12 weeks developed insulin resistance as measured by oral glucose tolerance test (Area under curve (AUC) mmol/L х min = 437±70 and 438±57) as compared to the C57BL/6 mice fed low or high fat diets (AUC mmol/L х min = 251±27 and 245±43). Arterial stiffness was determined by Doppler pulse wave velocity analysis of the femoral artery. Pulse wave velocity was increased in APN KO mice fed a high fat diet relative to those fed the low fat diet (12.56±0.78 cm/s vs 9.47±0.95 cm/s, p=0.0035; n=8-10). Pulse wave velocity was not different between C57BL/6 control mice on the low or high fat diets (10.63±0.73 cm/s and 10.86±0.50 cm/s), thus revealing that only mice deficient in adiponectin developed arterial stiffness in response to high fat diet. Conclusions: Potentiation of the vascular stiffness in diet-induced obese APN KO mice indicates that adiponectin has a role in modulating vascular structure and the APN KO mouse models the vascular changes that occur in human obesity and metabolic disorders. Morphometric analysis of the aortic tissues for vessel thickness and expression of extracellular proteins will further validate the potential role of adiponectin on the maintenance of arterial elasticity in addition to its known effect on eNOS mediated vasoprotection.


2018 ◽  
Vol 16 ◽  
pp. 205873921876094 ◽  
Author(s):  
Gang Yu ◽  
Lili Zhu ◽  
Haiyan Li ◽  
Youyou Shao ◽  
Lei Chong ◽  
...  

Overweight/obesity has been suggested as a risk factor for asthma development, and prospective studies have confirmed that high body weight precedes asthma symptoms. However, the nature of the association between overweight/obese status and asthma remains unclear. Animal models of obesity-related asthma are very useful for understanding disease pathophysiology. Although C57/B6J mice are the most widely used animal model for researching obesity-related asthma, gender differences are not always taken into consideration. Therefore, to explore the effect of gender on the development of obesity-related asthma, both female and male C57/B6J mice were used in this study. The mice were fed with a high-fat diet or a low-fat diet as control. Body weight, body length, liver weight, and Lee’s Index were used to evaluate obesity status, and lung histology, lung inflammatory cells infiltration, and inflammatory cytokines in bronchoalveolar lavage fluid (BALF) were examined for asthma evaluation. We found that the mean body weight of male mice on a high-fat diet gradually increased and was significantly higher than control male mice on a low-fat diet ( P < 0.01), while no significant differences were found between female mice at the end of 12 weeks of feeding. Furthermore, the obese asthma group female and male mice exhibited significantly high inflammatory cells infiltration than normal weight or obese female and male mice ( P < 0.01). However, the obese asthma group presented higher Neu infiltration, Th1 cytokine, and interferon gamma (IFNγ) concentrations in BALF than the asthma group in both the genders ( P < 0.01). In conclusion, both female and male mice are suitable for the obesity-related asthma model, although male mice might be more stable. Besides, obesity-related asthma is not Th2 type asthma.


2008 ◽  
Vol 15 (04) ◽  
pp. 500-507
Author(s):  
MUHAMMAD ANWAR BURIRO ◽  
MUHAMMAD TAYYAB

Objective: To determine the effects of Nigella sativa and sunflower oil diet intake on serum lipid profile in albino rats. Material& Methods: Eighty four albino rats with equal number of males and females were selected for the study, they were divided into six differentgroups, Control groups1,111,V,were given low fat diet(3%),high fat diet(20%), high fat diet supplemented with bile salt (1% colic acid) andantithyroid drug (0.5% propylthiouracil). The Experimental groups were given the above diets with supplemented Nigella sativa. Low fat dietincreased all the lipid fractions significantly when given at12 and 24 weeks duration as compared to 0 week. Results: The high fat diet whengiven at different intervals decreased all lipid fractions significantly as compared to baseline level. The high fat diet with propylthiouracil andbile salt also increased all the lipid fractions and the increase was more as compared to previous groups. The supplements of Nigella sativain the groups decreased all the lipid fractions significantly as compared to the control groups except HDL-c, which was significantly increasedin all the experimental groups as compared to control groups. Conclusion: On the basis of these findings conclusions are made, that Nigellasativa has got TG,TC, and LDL-c lowering and HDL-c raising effects.3% sunflower oil low fat diet has got TG,TC,HDL-c, and LDL-c raisingeffects.20% sunflower oil high fat diet has got TG,TC,HDL-c and LDL-c lowering effects. Both Nigella sativa and sunflower oil have got lowatherogenic index (TC/HDL) and may be recommended in hyperlipidaemic patients or normal individuals.


2019 ◽  
Vol 317 (2) ◽  
pp. E298-E311 ◽  
Author(s):  
Colin S. McCoin ◽  
Alex Von Schulze ◽  
Julie Allen ◽  
Kelly N. Z. Fuller ◽  
Qing Xia ◽  
...  

The impact of sexual dimorphism and mitophagy on hepatic mitochondrial adaptations during the treatment of steatosis with physical activity are largely unknown. Here, we tested if deficiencies in liver-specific peroxisome proliferative activated-receptor-γ coactivator-1α (PGC-1α), a transcriptional coactivator of biogenesis, and BCL-2/ADENOVIRUS EIB 19-kDa interacting protein (BNIP3), a mitophagy regulator, would impact hepatic mitochondrial adaptations (respiratory capacity, H2O2production, mitophagy) to a high-fat diet (HFD) and HFD plus physical activity via voluntary wheel running (VWR) in both sexes. Male and female wild-type (WT), liver-specific PGC-1α heterozygote (LPGC-1α), and BNIP3 null mice were thermoneutral housed (29–31°C) and divided into three groups: sedentary-low-fat diet (LFD), 16 wk of (HFD), or 16 wk of HFD with VWR for the final 8 wk (HFD + VWR) ( n = 5–7/sex/group). HFD did not impair mitochondrial respiratory capacity or coupling in any group; however, HFD + VWR significantly increased maximal respiratory capacity only in WT and PGC-1α females. Males required VWR to elicit mitochondrial adaptations that were inherently present in sedentary females including greater mitochondrial coupling control and reduced H2O2production. Females had overall reduced markers of mitophagy, steatosis, and liver damage. Steatosis and markers of liver injury were present in sedentary male mice on the HFD and were effectively reduced with VWR despite no resolution of steatosis. Overall, reductions in PGC-1α and loss of BNIP3 only modestly impacted mitochondrial adaptations to HFD and HFD + VWR with the biggest effect seen in BNIP3 females. In conclusion, hepatic mitochondrial adaptations to HFD and treatment of HFD-induced steatosis with VWR are more dependent on sex than PGC-1α or BNIP3.


1992 ◽  
Vol 263 (4) ◽  
pp. R785-R789 ◽  
Author(s):  
T. A. Buchanan ◽  
J. S. Fisler ◽  
S. Underberger ◽  
G. F. Sipos ◽  
G. A. Bray

To determine whether whole body insulin sensitivity differs between a rat strain that does not (S 5B/Pl) and a strain that does [Osborne-Mendel (OM)] become obese when eating a high-fat diet, we performed euglycemic clamp studies in animals from each strain during low- and high-fat feeding. Clamps were performed after 2 days ("initial clamp") and 9 days ("final clamp") on each diet. Plasma glucose and insulin levels during the final 60 min of initial and final clamps were similar in S 5B/Pl and OM rats regardless of diet. Insulin sensitivity, measured as the glucose clearance rate during the final 60 min of the clamp, averaged 35 +/- 3 ml.kg-1.min-1 in S 5B/Pl rats after 2 days on a low-fat diet. This did not change significantly during an additional 7 days on the low-fat diet. The high-fat diet was associated with a 13% reduction in insulin sensitivity after 2 days and a 30% reduction after 9 days in S 5B/Pl rats. OM rats exhibited similar patterns of insulin sensitivity during low- and high-fat diets, albeit at lower insulin sensitivity overall (P < 0.0005 vs. S 5B/Pl). Mean glucose clearance after 2 days on the low-fat diet was 27 +/- 2 mg.kg-1.min-1 and did not change significantly during seven more days of low-fat feeding. The high-fat diet was associated with a 19% reduction in glucose clearance after 2 days and a 38% reduction after 9 days in OM rats. The magnitude of reduction in insulin sensitivity during high-fat diets did not differ significantly between strains.(ABSTRACT TRUNCATED AT 250 WORDS)


2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 1699-1699
Author(s):  
Yanwen Wang ◽  
Sandhya Nair ◽  
Jacques Gagnon

Abstract Objectives The present study was designed to examine the effect of herring milt dry powder (HMDP) on glucose homeostasis and related metabolic phenotypes and compare its efficacy with herring milt protein hydrolysate (HMPH) in diet-induced obese and insulin resistant mice. Methods Male C57BL/6 J mice were pretreated with a high-fat diet for 7 weeks were divided into 3 groups where one group continued on the high-fat diet and used as the obese and insulin resistant control (HFC) and the other two groups were fed a modified HFC diet where 70% of casein was replaced with an equal percentage of protein derived from HMDP or HMPH. A group of mice fed a low-fat diet all the time was used as the normal or low-fat control (LFC). Body weight was obtained weekly and food intake was recorded daily. Semi-fating (4–6 hr) blood glucose was measured every other week using a glucometer using the blood from tail vein. Oral glucose tolerance was measured twice during weeks 5 and 9, respectively, and insulin tolerance was determined during week 7 of the treatment. At the end of the experiment, serum was obtained following overnight fasting for the measurement of fasting insulin, leptin, free fatty acids and lipids as well as other glucose metabolism-related biomarkers. Results During the 9-week treatment period, mice on the high-fat diet maintained significantly higher body weight and semi-fasting blood glucose levels and exhibited impaired oral glucose tolerance and insulin resistance relative to mice on the low-fat diet. At the end of the study, the analysis of fasting blood samples revealed that mice on the high-fat diet had increases in serum insulin, leptin, free fatty acids and cholesterol levels. Mice fed the high-fat diet also showed an increase in insulin resistance index and a decrease in β-cell function index. Compared to mice on the high-fat diet, the 70% replacement of dietary casein with an equal percentage of protein derived from HMDP or HMPH reversed or markedly improved these parameters, and HMDP and HMPH showed similar effects. Conclusions The results demonstrate that replacing dietary casein with the same amount of protein derived from either HMDP or HMPH prevents and improves high-fat-diet-induced obesity and insulin resistance. Funding Sources Atlantic Canada Opportunity Agency through the Atlantic Innovation Fund grant (no. 193,594) and National Research Council of Canada – NHP program.


2020 ◽  
Vol 96 (6) ◽  
Author(s):  
Sarah L Becker ◽  
Edna Chiang ◽  
Anna Plantinga ◽  
Hannah V Carey ◽  
Garret Suen ◽  
...  

ABSTRACT Artificial sweeteners have been shown to induce glucose intolerance by altering the gut microbiota; however, little is known about the effect of stevia. Here, we investigate whether stevia supplementation induces glucose intolerance by altering the gut microbiota in mice, hypothesizing that stevia would correct high fat diet-induced glucose intolerance and alter the gut microbiota. Mice were split into four treatment groups: low fat, high fat, high fat + saccharin and high fat + stevia. After 10 weeks of treatment, mice consuming a high fat diet (60% kcal from fat) developed glucose intolerance and gained more weight than mice consuming a low fat diet. Stevia supplementation did not impact body weight or glucose intolerance. Differences in species richness and relative abundances of several phyla were observed in low fat groups compared to high fat, stevia and saccharin. We identified two operational taxonomic groups that contributed to differences in beta-diversity between the stevia and saccharin groups: Lactococcus and Akkermansia in females and Lactococcus in males. Our results demonstrate that stevia does not rescue high fat diet-induced changes in glucose tolerance or the microbiota, and that stevia results in similar alterations to the gut microbiota as saccharin when administered in concordance with a high fat diet.


2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Luanfeng Wang ◽  
Bo Ren ◽  
Zhigang Liu ◽  
Xuebo Liu

Abstract Objectives Methionine restriction (MR) has emerged as a promising dietary restriction on metabolic syndrome as its beneficial effects on increasing metabolic flexibility and up-regulating mitochondrial function. The circadian clock directs many aspects of metabolism and macronutrients can function as zeitgebers for the clock in a tissue-specific way. It has been demonstrated that high-fat diet could alter daily oscillations via gut-brain axis. We hypothesis that MR is a new strategy could reverse the high-fat diet induced circadian rhythm disorders and cognitive impairments. Methods 3 month-old male C57BL/6 J mice were assigned to four groups based on diet: low-fat diet (0.86% methionine), low-fat diet with MR(0.17% methionine), high-fat diet, and high-fat diet with MR. After 8 weeks treatment, we employed behavioral test, transmission electron microscope, and 16S rDNA sequencing to evaluate cognitive function, rhythmic variation and the interconnection between gut microbiota and central nervous system. Results MR diminished HFD-induced body weight gain and restored the glucose tolerance at ZT0 (light phase) and ZT12 (dark phase). The neuroprotective effects of MR were connected with the ERK/CREB/BDNF signaling pathway and synaptic plasticity. MR changed energy metabolism via activated mTOR/ULK/AMPK signaling in brain. MR ameliorated rhythmic oscillations of clock control gene Bmal1/Per2 in gut-brain axis. Moreover, MR attenuated HFD-induced intestinal inflammatory and protected gut barrier integrity via enhancing the expression of intestinal tight junction protein. The gut microbiome was re-shaped by MR treatment, accompanied by the alteration of short chain fatty acids, the microbial products mediating systemic metabolism and has benefits on brain function. MR increased microbiota-derived butyric and isovaleric which possible synchronizers of peripheral circadian clocks. Conclusions The present study provided comprehensive evidence that MR attenuated obesity-induced cognitive impairment via balancing the circadian rhythm in gut-brain axis and that is a potential new therapeutic avenue for treating metabolic syndrome-related neurodegenerative diseases. Funding Sources This work was financially supported by the National Key Research and Development Program of China, National Natural Science Foundation of China. Supporting Tables, Images and/or Graphs


2001 ◽  
Vol 280 (2) ◽  
pp. R504-R509 ◽  
Author(s):  
L. Lin ◽  
R. Martin ◽  
A. O. Schaffhauser ◽  
D. A. York

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.


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