Host genetics and diet composition interact to modulate gut microbiota and predisposition to metabolic syndrome in spontaneously hypertensive stroke‐prone rats

Singh, Avninder; Zapata, Rizaldy C.; Pezeshki, Adel; Workentine, Matthew L.; Chelikani, Prasanth

doi:10.1096/fj.201801627rrr

Cited by 17 publications

(13 citation statements)

References 94 publications

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“…In a separate cohort of chow‐fed rats (n = 6/group), the volume of oxygen consumed (VO2, mL/kg body weight/h) and carbon dioxide produced (VCO2, mL/kg body weight/h) were continuously recorded at 12‐minutes intervals by indirect calorimetry (CLAMS setup; 2‐L/min flow) following a previously published protocol 111 . The total energy expenditure was computed using the following equation: 3.815 × VO2 (L/h) + 1.232 × VCO2 (L/h), and data were represented as kcal/h.…”

Section: Methodsmentioning

confidence: 99%

Intact vagal gut‐brain signalling prevents hyperphagia and excessive weight gain in response to high‐fat high‐sugar diet

et al. 2020

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Aim The tools that have been used to assess the function of the vagus nerve lack specificity. This could explain discrepancies about the role of vagal gut‐brain signalling in long‐term control of energy balance. Here we use a validated approach to selectively ablate sensory vagal neurones that innervate the gut to determine the role of vagal gut‐brain signalling in the control of food intake, energy expenditure and glucose homoeostasis in response to different diets. Methods Rat nodose ganglia were injected bilaterally with either the neurotoxin saporin conjugated to the gastrointestinal hormone cholecystokinin (CCK), or unconjugated saporin as a control. Food intake, body weight, glucose tolerance and energy expenditure were measured in both groups in response to chow or high‐fat high‐sugar (HFHS) diet. Willingness to work for fat or sugar was assessed by progressive ratio for orally administered solutions, while post‐ingestive feedback was tested by measuring food intake after an isocaloric lipid or sucrose pre‐load. Results Vagal deafferentation of the gut increases meal number in lean chow‐fed rats. Switching to a HFHS diet exacerbates overeating and body weight gain. The breakpoint for sugar or fat solution did not differ between groups, suggesting that increased palatability may not drive HFHS‐induced hyperphagia. Instead, decreased satiation in response to intra‐gastric infusion of fat, but not sugar, promotes hyperphagia in CCK‐Saporin‐treated rats fed with HFHS diet. Conclusions We conclude that intact sensory vagal neurones prevent hyperphagia and exacerbation of weight gain in response to a HFHS diet by promoting lipid‐mediated satiation.

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Section: Methodsmentioning

confidence: 99%

Intact vagal gut‐brain signalling prevents hyperphagia and excessive weight gain in response to high‐fat high‐sugar diet

et al. 2020

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“…Except for affording more energy, it was found that a high-fat diet diminished gut barrier-protecting bacteria and enriched endotoxin producers (Chassaing et al, 2015) to induce lipid accumulation (Faillaci et al, 2018). Although the intestinal microbiota is influenced by diet components, there is a substantial interindividual variation in the intestinal bacterial composition in response to diets, suggesting the genetic factor should not be ignored when we evaluate the metabolic characteristics (Ussar et al, 2016;Singh et al, 2019). Kreznar et al (2017) characterized the metabolic phenotypes of eight genetically distinct inbred mouse strains in response to a high energy diet and found that different mouse strains showed great variation in the intestinal microbiota as well as the diabetesrelated phenotypes, showing the dominant role of genetic factors in shaping the intestinal microbiota.…”

Section: Introductionmentioning

confidence: 99%

Alteration and the Function of Intestinal Microbiota in High-Fat-Diet- or Genetics-Induced Lipid Accumulation

Qiao

Tan

et al. 2021

Front. Microbiol.

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Diet and host genetics influence the composition of intestinal microbiota, yet few studies have compared the function of intestinal microbiota in the diet- or genotype-induced lipid deposition, which limits our understanding of the role of intestinal bacteria in metabolic disorders. The lipid accumulation in wild-type zebrafish fed with control (CON) or high-fat (HF) diet and two gene-knockout zebrafish lines (cpt1b–/– or pparab–/–) fed with control diet was measured after a 4-week feeding experiment. The intestinal microbiota composition of these groups was investigated using 16S ribosomal RNA (rRNA) gene sequencing (DNA-based) and 16S rRNA sequencing (RNA-based). The HF diet or deficiency of two genes induced more weight gain and higher triglyceride content in the liver compared with their control group. 16S rRNA gene sequencing (DNA-based) indicated the decreased abundance of Proteobacteria in the HF group compared with CON, but there was no significant difference in bacterial α diversity among treatments. 16S rRNA sequencing (RNA-based) confirmed the decreased abundance of Proteobacteria and the bacterial α diversity in the HF group compared with CON. Deficiency of cpt1b or pparab showed less change in microbiota composition compared with their wild-type group. Intestinal microbiota of each group was transferred to germ-free zebrafish, and the quantification of Nile red staining indicated that the intestinal microbiota of the HF group induced more lipid accumulation compared with CON, whereas intestinal microbiota of cpt1b–/– and pparab–/– zebrafish did not. The results showed that RNA-based bacterial sequencing revealed more bacterial alteration than DNA-based bacterial sequencing. HF diet had a more dominant role in shaping gut microbiota composition to induce lipid accumulation compared with the gene-knockout of cpt1b or pparab in zebrafish, and the transplant of intestinal microbiota from HF-fed fish induced more lipid deposition in germ-free zebrafish. Together, these data suggested that a high-fat diet exerted a more dominant role over the deletion of cpt1b or pparab on the intestinal bacterial composition, which corresponded to lipid accumulation.

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“…The intestinal (gut) microbiota is an important environmental factor that plays a key role in development of obesity and diabetes . The trillions of microbes present in the intestinal tract form a complex system, and physiological state is modulated by interactions between microbiota and the host .…”

Section: Introductionmentioning

confidence: 99%

“…3,4 The trillions of microbes present in the intestinal tract form a complex system, and physiological state is modulated by interactions between microbiota and the host. 3,4 The trillions of microbes present in the intestinal tract form a complex system, and physiological state is modulated by interactions between microbiota and the host.…”

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confidence: 99%

Phellinus linteus polysaccharide extract improves insulin resistance by regulating gut microbiota composition

Liu

Wang

et al. 2019

FASEB j.

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The hypoglycemic effect of Phellinus linteus polysaccharide extract (PLPE) has been documented in several previous studies, but the functional interactions among PLPE, gut microbiota, and the hypoglycemic effect remain unclear. We examined the regulatory effect of PLPE on gut microbiota, and the molecular mechanism underlying improvement of insulin resistance, using a type 2 diabetic rat model. Here, 24 male Sprague‐Dawley rats were randomly divided into four groups that were subjected to intervention of saline (normal and model control group), metformin (120 mg/kg.bw), and PLPE (600 mg/kg.bw) by oral administration. After 8 weeks of treatment, PLPE increased levels of short‐chain fatty acids (SCFAs) by enhancing abundance of SCFA‐producing bacteria. SCFAs maintained intestinal barrier function and reduced lipopolysaccharides content in blood, thereby helping to reduce systemic inflammation and reverse insulin resistance. Our findings suggest that PLPE (in which polysaccharides are the major component) has potential application as a prebiotic for regulating gut microbiota composition in diabetic patients.

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Host genetics and diet composition interact to modulate gut microbiota and predisposition to metabolic syndrome in spontaneously hypertensive stroke‐prone rats

Cited by 17 publications

References 94 publications

Intact vagal gut‐brain signalling prevents hyperphagia and excessive weight gain in response to high‐fat high‐sugar diet

Intact vagal gut‐brain signalling prevents hyperphagia and excessive weight gain in response to high‐fat high‐sugar diet

Alteration and the Function of Intestinal Microbiota in High-Fat-Diet- or Genetics-Induced Lipid Accumulation

Phellinus linteus polysaccharide extract improves insulin resistance by regulating gut microbiota composition

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