scholarly journals 2′-Fucosyllactose Supplementation Improves Gut-Brain Signaling and Diet-Induced Obese Phenotype and Changes the Gut Microbiota in High Fat-Fed Mice

Nutrients ◽  
2020 ◽  
Vol 12 (4) ◽  
pp. 1003 ◽  
Author(s):  
Sunhye Lee ◽  
Michael Goodson ◽  
Wendie Vang ◽  
Karen Kalanetra ◽  
Daniela Barile ◽  
...  

Obesity is characterized by fat accumulation, chronic inflammation and impaired satiety signaling, which may be due in part to gut microbial dysbiosis. Manipulations of the gut microbiota and its metabolites are attractive targets for obesity treatment. The predominant oligosaccharide found in human milk, acts as a prebiotic with beneficial effects on the host. However, little is known about the beneficial effects of 2′-FL in obesity. The aim of this study was to determine the beneficial effects of 2′-FL supplementation on the microbiota-gut-brain axis and the diet-induced obese phenotype in high fat (HF)-fed mice. Male C57/BL6 mice (n = 6/group; six weeks old) were counter-balanced into six weight-matched groups and fed either a low-fat (LF; 10% kcal as fat), HF (45% kcal as fat) or HF diet with 2′-FL (HF_2′-FL) at 1, 2, 5 and 10% (w/v) in drinking water for six weeks. General phenotypes (body weight, energy intake, fat and lean mass), cecal microbiome and metabolites, gut-brain signaling, intestinal permeability and inflammatory and lipid profiles were assessed. Only 10% 2′-FL, but not 1, 2 or 5%, decreased HF diet-induced increases in energy intake, fat mass and body weight gain. A supplementation of 10% 2′-FL changed the composition of cecal microbiota and metabolites compared to LF- and HF-fed mice with an increase in Parabacteroides abundance and lactate and pyruvate, respectively, whose metabolic effects corresponded to our study findings. In particular, 10% 2′-FL significantly reversed the HF diet-induced impairment of cholecystokinin-induced inhibition of food intake. Gene expressions of interleukin (IL)-1β, IL-6, and macrophage chemoattractant protein-1 in the cecum were significantly downregulated by 10% 2′-FL compared to the HF group. Furthermore, 10% 2′-FL suppressed HF diet-induced upregulation of hepatic peroxisome proliferator-activated receptor gamma, a transcription factor for adipogenesis, at the gene level. In conclusion, 10% 2′-FL led to compositional changes in gut microbiota and metabolites associated with improvements in metabolic profiles and gut-brain signaling in HF-fed mice. These findings support the use of 2′-FL for modulating the hyperphagic response to HF diets and improving the microbiota-gut-brain axis.

2007 ◽  
Vol 97 (2) ◽  
pp. 389-398 ◽  
Author(s):  
Patricia Pérez-Matute ◽  
Nerea Pérez-Echarri ◽  
J. Alfredo Martínez ◽  
Amelia Marti ◽  
María J. Moreno-Aliaga

n-3 PUFA have shown potential anti-obesity and insulin-sensitising properties. However, the mechanisms involved are not clearly established. The aim of the present study was to assess the effects of EPA administration, one of the n-3 PUFA, on body-weight gain and adiposity in rats fed on a standard or a high-fat (cafeteria) diet. The actions on white adipose tissue lipolysis, apoptosis and on several genes related to obesity and insulin resistance were also studied. Control and cafeteria-induced overweight male Wistar rats were assigned into two subgroups, one of them daily received EPA ethyl ester (1 g/kg) for 5 weeks by oral administration. The high-fat diet induced a very significant increase in both body weight and fat mass. Rats fed with the cafeteria diet and orally treated with EPA showed a marginally lower body-weight gain (P = 0·09), a decrease in food intake (P < 0·01) and an increase in leptin production (P < 0·05). EPA administration reduced retroperitoneal adipose tissue weight (P < 0·05) which could be secondary to the inhibition of the adipogenic transcription factor PPARγ gene expression (P < 0·001), and also to the increase in apoptosis (P < 0·05) found in rats fed with a control diet. TNFα gene expression was significantly increased (P < 0·05) by the cafeteria diet, while EPA treatment was able to prevent (P < 0·01) the rise in this inflammatory cytokine. Adiposity-corrected adiponectin plasma levels were increased by EPA. These actions on both TNFα and adiponectin could explain the beneficial effects of EPA on insulin resistance induced by the cafeteria diet.


2020 ◽  
Vol 124 (4) ◽  
pp. 396-406 ◽  
Author(s):  
Hongyang Yao ◽  
Chaonan Fan ◽  
Xiuqin Fan ◽  
Yuanyuan Lu ◽  
Yuanyuan Wang ◽  
...  

AbstractAberration in leptin expression is one of the most frequent features in the onset and progression of obesity, but the underlying mechanisms are still unclear and need to be clarified. This study investigated the effects of the absence of gut microbiota on body weight and the expression and promoter methylation of the leptin. Male C57 BL/6 J germ-free (GF) and conventional (CV) mice (aged 4–5 weeks) were fed either a normal-fat diet (NFD) or a high-fat diet (HFD) for 16 weeks. Six to eight mice from each group, at 15 weeks, were administered exogenous leptin for 7 d. Leptin expression and body weight gain in GF mice were increased by NFD with more CpG sites hypermethylated at the leptin promoter, whereas there was no change with HFD, compared with CV mice. Adipose or hepatic expression of genes associated with fat synthesis (Acc1, Fas and Srebp-1c), hydrolysis and oxidation (Atgl, Cpt1a, Cpt1c, Ppar-α and Pgc-1α) was lower, and hypothalamus expression of Pomc and Socs3 was higher in GF mice than levels in CV mice, particularly with NFD feeding. Exogenous leptin reduced body weight in both types of mice, with a greater effect on CV mice with NFD. Adipose Lep-R expression was up-regulated, and hepatic Fas and hypothalamic Socs3 were down-regulated in both types of mice. Expression of fat hydrolysis and oxidative genes (Atgl, Hsl, Cpt1a, Cpt1c, Ppar-α and Pgc-1α) was up-regulated in CV mice. Therefore, the effects of gut microbiota on the leptin expression and body weight were affected by dietary fat intake.


2019 ◽  
Author(s):  
Kathleen E. Morrison ◽  
Eldin Jašarević ◽  
Christopher D. Howard ◽  
Tracy L. Bale

AbstractBackgroundDietary effects on the gut microbiome has been shown to play a key role in the pathophysiology of behavioral dysregulation, inflammatory disorders, metabolic syndrome, and obesity. Often overlooked is that experimental diets vary significantly in the proportion and source of dietary fiber. Commonly, treatment comparisons are made between animals that are fed refined diets that lack soluble fiber and animals fed vivarium-provided chow diet that contain a rich source of soluble fiber. Despite the well-established role of soluble fiber on metabolism, immunity, and behavior via the gut microbiome, the extent to which measured outcomes may be driven by differences in dietary fiber is unclear. Further, the significant impact of sex and age in response to dietary challenge is likely important and should also be considered.ResultsWe compared the impact of transitioning young and aged male and female mice from a chow diet to a refined low soluble fiber diet on body weight and gut microbiota. Then, to determine the contribution of dietary fat, we examined the impact of transitioning a subset of animals from refined low fat to refined high fat diet. Serial tracking of body weights revealed that consumption of low fat or high fat refined diet increased body weight in young and aged adult male mice. Young adult females showed resistance to body weight gain, while high fat diet-fed aged females had significant body weight gain. Transition from a chow diet to low soluble fiber refined diet accounted for most of the variance in community structure and composition across all groups. This dietary transition was characterized by a loss of taxa within the phylum Bacteroidetes and a concurrent bloom of Clostridia and Proteobacteria in a sex- and age-specific manner. Most notably, no changes to gut microbiota community structure and composition were observed between mice consuming either low- or high-fat diet, suggesting that transition to the refined diet that lacks soluble fiber is the primary driver of gut microbiota alterations, with limited additional impact of dietary fat on gut microbiota.ConclusionCollectively, our results show that the choice of control diet has a significant impact on outcomes and interpretation related to body weight and gut microbiota. These data also have broad implications for rodent studies that draw comparisons between refined high fat diets and chow diets to examine dietary fat effects on metabolic, immune, behavioral, and neurobiological outcomes.


2022 ◽  
Vol 88 ◽  
pp. 104869
Author(s):  
Ju Kyoung Oh ◽  
Robie Vasquez ◽  
Sang Hoon Kim ◽  
Je Hyeon Lee ◽  
Eun Joo Kim ◽  
...  

2021 ◽  
Author(s):  
Tanja Jene ◽  
Inigo Ruiz de Azua ◽  
Annika Hasch ◽  
Jennifer Klüpfel ◽  
Julia Deuster ◽  
...  

Stress has a major impact on the modulation of metabolism, as previously evidenced by hyperglycemia following chronic social defeat (CSD) stress in mice. Although CSD-triggered metabolic dysregulation might predispose to pre-diabetic conditions, insulin sensitivity remained intact, and obesity did not develop, when animals were fed with a standard diet (SD). Here, we investigated whether a nutritional challenge, a high fat diet (HFD), aggravates the metabolic phenotype, and whether there are particularly sensitive time windows for the negative consequences of HFD exposure. Chronically stressed male mice and controls (CTRL) were kept under (i) SD-conditions, (ii) with HFD commencing post-CSD, or (iii) provided with HFD lasting throughout, and after CSD. Under SD conditions, stress increased glucose levels early post-CSD. Both HFD regimens increased glucose levels in non-stressed mice, but not in stressed mice. Nonetheless, when HFD was provided after CSD, stressed mice did not differ from controls in long-term body weight gain, fat tissue mass and plasma insulin, and leptin levels. In contrast, when HFD was continuously available, stressed mice displayed reduced body weight gain, lowered plasma levels of insulin, and leptin, and reduced white adipose tissue weights as compared to their HFD-treated non-stressed controls. Interestingly, stress-induced adrenal hyperplasia and hypercortisolemia were observed in mice treated with SD and with HFD after CSD, but not in stressed mice exposed to a continuous HFD treatment. The present work demonstrates that CSD can reduce HFD-induced metabolic dysregulation. Hence, HFD during stress may act beneficially, as comfort food, by decreasing stress-induced metabolic demands.


2020 ◽  
Author(s):  
Geok Hun Tan ◽  
Mohd Shaufi Mohd Asrore ◽  
Abdul Rahman Omar ◽  
Chun Wie Chong

Abstract Background Probiotics are the most recognised alternative to antibiotic growth promoters (AGPs) for poultry production. They adhere to the intestinal epithelial cells to exert their beneficial effects on the host. However, this is often restricted by indigenous gut microbes that compete for adhesion sites and nutrients. Therefore, phage application has been proposed to reduce the competition of probiotics with gut microbiota. The main objective of this study was to investigate the effects of phages on the gut microbiota and their impact on probiotic efficacy in chickens. Results Four best Escherichia coli lytic phages were selected and characterised. The in vivo trial was conducted to investigate the effects of dietary treatments of phage cocktail at 0.1% (1ɸ) and 0.2% (2ɸ), 0.1% PrimaLac ® probiotic (P) and their combinations (1ɸP, 2ɸP) on growth performance and gut microbiota of chickens. The results from the in vivo trial showed that chickens in the 1ɸP group had significantly (P < 0.05) better body weight (BW), body weight gain (BWG), and feed conversion ratio (FCR), lower serum triglycerides and higher ileal villus height than the control. Chickens in the 1ɸP group also had higher (P < 0.05) ileal villus height, and lower crypt depth than those in the probiotic group. The gut microbiota profiles revealed that 1ɸP supplementation significantly (P < 0.05) reduced E. coli population, increased (P < 0.001) short chain fatty acids (SCFAs) producers, and improved (P < 0.001) gene expressions that are related to carbohydrate and amino acid metabolisms, and nutrient uptake. Conclusions The results from this study showed that 1ɸP treatment could modulate the gut microbiota and enhance growth performance in chickens. This finding could be considered as a potential alternative to AGPs for poultry.


2000 ◽  
Vol 83 (S1) ◽  
pp. S33-S38 ◽  
Author(s):  
John E. Blundell ◽  
John Cooling

Gain in body weight over a number of years could be achieved through cumulative positive energy balances. These positive balances could come about through adjustments in the various components of energy expenditure or fuel utilization, together with shifts in food selection or eating patterns leading to adjustments in macronutrient intake. This means that many combinations of intake and expenditure could lead to a positive energy balance; these combinations can be called routes to body weight gain. However, these routes are difficult to trace by studying random samples of individuals. Previous investigations have found a clear association between high fat consumption and the occurrence of obesity, and although a high fat intake is a strong behavioural risk factor for weight gain, the relationship does not constitute a biological inevitability. Some normal-weight and lean individuals appear to eat a high-fat diet. To investigate reasons for this we have studied individuals initially defined by particular clusters of dietary characteristics related to fat and carbohydrate consumption. Habitual high-fat (HF) and low-fat (LF) consumers have been termed phenotypes. Various aspects of energy expenditure (physiological and behavioural) and energy intake were measured in these individuals with contrasting profiles. HF phenotypes had high intakes of fatty foods and an overall higher energy intake than LF. However, these groups of young adult males had similar BMIs and percentage body fat. The HF had a significantly higher resting metabolic rate (RMR) and a lower RQ, together with high plasma fasting leptin levels, and a higher sleeping heart rate. In HF individuals the physical activity level was somewhat lower and they had significantly more periods of sedentary behaviour than LF subjects. Although HF individuals appear to be more vulnerable to developing obesity, both phenotypes carry particular risk factors and protective factors for weight gain. The use of phenotypes has allowed the identification of different potential routes to weight gain. Different strategies are required to prevent age-related increase in body weight in these quite different individuals.


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