scholarly journals The Role of the Gut Microbiome in Energy Balance With a Focus on the Gut-Adipose Tissue Axis

2020 ◽  
Vol 11 ◽  
Author(s):  
Han Xiao ◽  
Sona Kang
2020 ◽  
Author(s):  
Aaron R. Cox ◽  
Natasha Chernis ◽  
Kang Ho Kim ◽  
Peter M. Masschelin ◽  
Pradip K. Saha ◽  
...  

ABSTRACTObjectiveWhite adipose tissue (WAT) expansion regulates energy balance and overall metabolic homeostasis. WAT absence or loss occurring through lipodystrophy and lipoatrophy contributes to the development of dyslipidemia, hepatic steatosis, and insulin resistance. We previously demonstrated the sole small ubiquitin-like modifier (SUMO) E2-conjuguating enzyme Ubc9 represses human adipocyte differentiation. Germline and other tissue-specific deletions of Ubc9 frequently cause lethality in mice. As a result, the role of Ubc9 during WAT development remains unknown.MethodsTo determine how Ubc9 impacts body composition and energy balance, we generated adipocyte-specific Ubc9 knockout mice (Ubc9a-KO). CRISPR/Cas9 gene editing inserted loxP sites flanking exons 3 and 4 at the Ubc9 locus. Subsequent genetic crosses to AdipoQ-Cre transgenic mice allowed deletion of Ubc9 in white and brown adipocytes. We measured multiple metabolic endpoints that describe energy balance and carbohydrate metabolism in Ubc9a-KO and littermate controls during postnatal growth.ResultsTo our surprise, Ubc9a-KO mice developed hyperinsulinemia and hepatic steatosis. Global energy balance defects emerged from dysfunctional WAT marked by pronounced local inflammation, loss of serum adipokines, hepatomegaly, and near absence of major adipose tissue depots. We observed progressive lipoatrophy that commences in the early adolescent period.ConclusionsOur results demonstrate that Ubc9 expression in mature adipocytes is essential for maintaining WAT expansion. Deletion of Ubc9 in fat cells compromised and diminished adipocyte function that provoked WAT inflammation and ectopic lipid accumulation in the liver. Our findings reveal an indispensable role for Ubc9 during white adipocyte expansion and endocrine control of energy balance.


Author(s):  
Ifeanyi O. Oshim ◽  
Nneka R. Agbakoba ◽  
Evelyn U. Urama ◽  
Oluwayemisi Odeyemi ◽  
Nkechi A. Olise ◽  
...  

Microbiome that reside in the human gut are key contributors to host metabolism and are considered potential sources of novel therapeutics in metabolic disorders. This review discusses the role of gut microbiome in the pathogenesis of obesity, type 2 diabetes mellitus (T2DM), chronic kidney disease and cardiovascular disease. Gut microbiome remains quite stable, although changes take place between birth and adulthood due to external influences, such as diet, disease and environment. Understanding these changes is important to predict diseases and develop therapies. In gut heamostasis, Gut microbiome converts high fibres intake into short-chain fatty acids like butyrate, propionate and acetate which normalize intestinal permeability and alter de novo lipogenesis and gluconeogenesis through reduction of free fatty acid production by visceral adipose tissue. This effect contributes to reduce food intake and to improve glucose metabolism. Propionate can also bind to G protein coupled receptors (GPR)-43 expressed on lymphocytes in order to maintain appropriate immune defence. Butyrate activates peroxisome proliferator-activated receptor-γ (PPAR-γ) leading to beta-oxidation and oxygen consumption, a phenomenon contributing to maintain anaerobic condition in the gut lumen. In contrast, diets most especially western diet consisting among others of high fat and high salt content has been reported to cause gut dysbiosis. This alteration of gut microbiome result to chronic bacterial translocation and increased intestinal permeability that can drive a systemic inflammation leading to macrophage influx into visceral adipose tissue, activation of hepatic kuffer cells and insulin resistance in type 2 diabetes. This effect contributes to lower mucus thickness, decrease butyrate and propionate producing bacteria, L-cells secrete less gut peptides, lack of PPAR-γ activation lead to higher oxygen available for the microbiome at the proximity of the mucosa and increases the proliferation of Enterobacteriaceae with commensurate increase in opportunistic pathogens. However, Gut microbiome are major biomarker for early prognosis of diabetes and other metabolic disorders.


2011 ◽  
Vol 16 (3) ◽  
pp. 139 ◽  
Author(s):  
Hyun-Ju Kim ◽  
Sang-Hyun Choi ◽  
Boe-Gwun Chun ◽  
Dong-Hoon Kim

2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
Shilpa Kshatriya ◽  
Kan Liu ◽  
Ali Salah ◽  
Tamas Szombathy ◽  
Ronald H. Freeman ◽  
...  

Leptin is a 16-kDa-peptide hormone that is primarily synthesized and secreted by adipose tissue. One of the major actions of this hormone is the control of energy balance by binding to receptors in the hypothalamus, leading to reduction in food intake and elevation in temperature and energy expenditure. In addition, increasing evidence suggests that leptin, through both direct and indirect mechanisms, may play an important role in cardiovascular and renal regulation. While the relevance of endogenous leptin needs further clarification, it appears to function as a pressure and volume-regulating factor under conditions of health. However, in abnormal situations characterized by chronic hyperleptinemia such as obesity, it may function pathophysiologically for the development of hypertension and possibly also for direct renal, vascular, and cardiac damage.


2019 ◽  
Vol 111 (2) ◽  
pp. 340-350 ◽  
Author(s):  
Amy Jennings ◽  
Manja Koch ◽  
Majken K Jensen ◽  
Corinna Bang ◽  
Jan Kassubek ◽  
...  

ABSTRACT Background Flavonoid intake modifies the composition of the gut microbiome, which contributes to the metabolism of flavonoids. Few studies have examined the contribution of the gut microbiome to the health benefits associated with flavonoid intake. Objectives We aimed to examine associations between habitual intakes of flavonoid subclasses and MRI-determined visceral (VAT) and subcutaneous (SAT) adipose tissue. Uniquely, we also identified associations between the aforementioned measurements and gut microbiome composition sequenced from 16S ribosomal RNA genes. Methods We undertook cross-sectional analyses of 618 men and women (n = 368 male), aged 25–83 y, from the PopGen cohort. Results Higher intake of anthocyanins was associated with lower amounts of VAT [tertile (T)3-T1:  −0.49 dm3; β: −8.9%; 95% CI: −16.2%, −1.1%; P = 0.03] and VAT:SAT ratio (T3-T1: −0.04; β: −7.1%; 95% CI: −13.5%, −0.3%; P = 0.03). Higher intakes of anthocyanin-rich foods were also inversely associated with VAT [quantile (Q)4-Q1: −0.39 dm3; β: −9.9%; 95% CI: −17.4%, −1.6%; P = 0.02] and VAT:SAT ratio (Q4-Q1: −0.04; β: −6.5%; 95% CI: −13.3%, −0.9%; P = 0.03). Participants with the highest intakes of anthocyanin-rich foods also had higher microbial diversity (Q4-Q1: β: 0.18; 95% CI: 0.06, 0.31; P < 0.01), higher abundances of Clostridiales (Q4-Q1: β: 449; 95% CI: 96.3, 801; P = 0.04) and Ruminococcaceae (Q4-Q1: β: 313; 95% CI: 33.6, 591; P = 0.04), and lower abundance of Clostridium XIVa (Q4-Q1: β: −41.1; 95% CI: −72.4, −9.8; P = 0.04). Participants with the highest microbial diversity, abundances of Clostridiales and Ruminococcaceae, and lower abundance of Clostridium XIVa had lower amounts of VAT. Up to 18.5% of the association between intake of anthocyanin-rich foods and VAT could be explained by the gut microbiome. Conclusions These novel data suggest that higher microbial diversity and abundance of specific taxa in the Clostridiales order may contribute to the association between higher intake of anthocyanins and lower abdominal adipose tissue.


2018 ◽  
Vol 315 (4) ◽  
pp. R708-R720 ◽  
Author(s):  
Jean-Philippe Krieger ◽  
Ellen Paula Santos da Conceição ◽  
Graciela Sanchez-Watts ◽  
Myrtha Arnold ◽  
Klaus G. Pettersen ◽  
...  

Endogenous intestinal glucagon-like peptide-1 (GLP-1) controls satiation and glucose metabolism via vagal afferent neurons (VANs). Recently, VANs have received increasing attention for their role in brown adipose tissue (BAT) thermogenesis. It is, however, unclear whether VAN GLP-1 receptor (GLP-1R) signaling affects BAT thermogenesis and energy expenditure (EE) and whether this VAN mechanism contributes to energy balance. First, we tested the effect of the GLP-1R agonist exendin-4 (Ex4, 0.3 μg/kg ip) on EE and BAT thermogenesis and whether these effects require VAN GLP-1R signaling using a rat model with a selective Glp1r knockdown (kd) in VANs. Second, we examined the role of VAN GLP-1R in energy balance during chronic high-fat diet (HFD) feeding in VAN Glp1r kd rats. Finally, we used viral transsynaptic tracers to identify the possible neuronal substrates of such a gut-BAT interaction. VAN Glp1r kd attenuated the acute suppressive effects of Ex4 on EE and BAT thermogenesis. Consistent with this finding, the VAN Glp1r kd increased EE and BAT activity, diminished body weight gain, and improved insulin sensitivity compared with HFD-fed controls. Anterograde transsynaptic viral tracing of VANs infected major hypothalamic and hindbrain areas involved in BAT sympathetic regulation. Moreover, retrograde tracing from BAT combined with laser capture microdissection revealed that a population of VANs expressing Glp1r is synaptically connected to the BAT. Our findings reveal a novel role of VAN GLP-1R signaling in the regulation of EE and BAT thermogenesis and imply that through this gut-brain-BAT connection, intestinal GLP-1 plays a role in HFD-induced metabolic syndrome.


1989 ◽  
Vol 67 (4) ◽  
pp. 369-369
Author(s):  
Denis Richard

Our knowledge of mammalian energetics has improved considerably during the last decade. Some twelve years ago energetics, which was a low priority research area (except perhaps for the agricultural nutritionists), started to revive with the publication of major contributions emphasizing the role of thermogenesis in the regulation of energy balance. Trayhum et al. (1979) observed that obesity in genetically obese mice was associated with a reduced energy expenditure for thermoregulatory thermogenesis. Meanwhile, Rothwell and Stock (1979) published results suggesting that the ability of young leanrats to resist obesity when made hyperphagic by palatable food was due to an increase in a facultative form of thermogenesis. Brown adipose tissue, which was recognized in the meantime as the main site of nonshivering thermogenesis in cold-adapted, cold-exposed rats (Foster and Frydman 1979), was also proposed as the major thermogenic effector in diet-induced thermogenesis. These studies attracted several researchers interested in understanding the etiology of obesity, an energy balance disorder that tends to be too often seen as merely the result of overfeeding. As a consequence, a tremendous amount of literature has emerged from a wide spectrum of disciplines. Although this literature supports the role of thermogenesis in energy balance of experimental animals, it does not provide all the mechanistic bases underlying this action. Besides, the role of thermogenesis in energy balance in man remains to be more firmly established. The present issue of the Canadian Journal of Physiology and Pharmacology contains a series of articles on the role of thermogenesis in energy balance. The following topics are reviewed: the role of thermogenesis in the regulation of energy balance in relation to obesity; the regulation of energy metabolism in diabetes; the role of brown adipose tissue in diet-induced thermogenesis; the role of exercise training in energy balance; and the role of thermogenesis in the energetics of pregnancy and lactation. These articles summarize the current views of some Canadian researchers who have actively contributed to the development of our knowledge on nutritional energetics during recent years.


1977 ◽  
Vol 36 ◽  
pp. 143-180 ◽  
Author(s):  
J.O. Stenflo

It is well-known that solar activity is basically caused by the Interaction of magnetic fields with convection and solar rotation, resulting in a great variety of dynamic phenomena, like flares, surges, sunspots, prominences, etc. Many conferences have been devoted to solar activity, including the role of magnetic fields. Similar attention has not been paid to the role of magnetic fields for the overall dynamics and energy balance of the solar atmosphere, related to the general problem of chromospheric and coronal heating. To penetrate this problem we have to focus our attention more on the physical conditions in the ‘quiet’ regions than on the conspicuous phenomena in active regions.


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