The changing microbial landscape of Western society: Diet, dwellings and discordance

Background: The last 50–100 years has been marked by a sharp rise in so-called “Western-diseases” in those countries that have experienced major industrial advances and shifts towards urbanized living. These diseases include obesity, type 2 diabetes, inflammatory bowel diseases, and food allergies in which chronic dysregulation of metabolic and/or immune processes appear to be involved, and are likely a byproduct of new environmental influences on our ancient genome. What we now appreciate is that this genome consists of both human and co-evolved microbial genes of the trillions of microbes residing in our body. Together, host–microbe interactions may be determined by the changing diets and behaviors of the Western lifestyle, influencing the etiopathogenesis of “new-age” diseases. Scope of review: This review takes an anthropological approach to the potential interplay of the host and its gut microbiome in the post-industrialization rise in chronic inflammatory and metabolic diseases. The discussion highlights both the changes in diet and the physical environment that have co-occurred with these diseases and the latest evidence demonstrating the role of host–microbe interactions in understanding biological responses to the changing environment. Major conclusions: Technological advances that have led to changes in agriculture and engineering have altered our eating and living behaviors in ways never before possible in human history. These changes also have altered the bacterial communities within the human body in ways that are seemingly linked with the rise of many intestinal and systemic metabolic and inflammatory diseases. Insights into the mechanisms of this reciprocal exchange between the environment and the human gut microbiome may offer potential to attenuate the chronic health conditions that derail quality of life. This article is part of a special issue on microbiota

The changing microbial landscape of Western society: Diet, dwellings and discordance.

BackgroundThe last 50-100 years has been marked by a sharp rise in so-called "Western-diseases" in those countries that have experienced major industrial advances and shifts towards urbanized living. These diseases include obesity, type 2 diabetes, inflammatory bowel diseases, and food allergies in which chronic dysregulation of metabolic and/or immune processes appear to be involved, and are likely a byproduct of new environmental influences on our ancient genome. What we now appreciate is that this genome consists of both human and co-evolved microbial genes of the trillions of microbes residing in our body. Together, host-microbe interactions may be determined by the changing diets and behaviors of the Western lifestyle, influencing the etiopathogenesis of "new-age" diseases.Scope of reviewThis review takes an anthropological approach to the potential interplay of the host and its gut microbiome in the post-industrialization rise in chronic inflammatory and metabolic diseases. The discussion highlights both the changes in diet and the physical environment that have co-occurred with these diseases and the latest evidence demonstrating the role of host-microbe interactions in understanding biological responses to the changing environment.Major conclusionsTechnological advances that have led to changes in agriculture and engineering have altered our eating and living behaviors in ways never before possible in human history. These changes also have altered the bacterial communities within the human body in ways that are seemingly linked with the rise of many intestinal and systemic metabolic and inflammatory diseases. Insights into the mechanisms of this reciprocal exchange between the environment and the human gut microbiome may offer potential to attenuate the chronic health conditions that derail quality of life. This article is part of a special issue on microbiota

Isoflurane and Sevoflurane Induce Severe Hepatic Insulin Resistance in a Canine Model

<div><p>Introduction</p><p>Anesthesia induces insulin resistance, which may contribute to elevated blood glucose and adverse post-operative outcomes in critically ill patients, and impair glycemic control in surgical patients with diabetes. However, little is known about the mechanisms by which anesthesia impairs insulin sensitivity. Here we investigate the effects of anesthesia on insulin sensitivity in metabolic tissues.</p><p>Methods</p><p>Hyperinsulinemic-euglycemic clamps were performed in 32 lean (control diet; n = 16 conscious versus n = 16 anesthetized) and 24 fat-fed (6 weeks fat-feeding; n = 16 conscious versus n = 8 anesthetized) adult male mongrel dogs in conjunction with tracer methodology to differentiate hepatic versus peripheral insulin sensitivity. Propofol was administered as an intravenous bolus (3mg/kg) to initiate anesthesia, which was then maintained with inhaled sevoflurane or isoflurane (2–3%) for the duration of the procedure.</p><p>Results</p><p>Anesthesia reduced peripheral insulin sensitivity by approximately 50% in both lean and fat-fed animals as compared to conscious animals, and insulin action at the liver was almost completely suppressed during anesthesia such that hepatic insulin sensitivity was decreased by 75.5% and; 116.2% in lean and fat-fed groups, respectively.</p><p>Conclusion</p><p>Inhaled anesthesia induces severe hepatic insulin resistance in a canine model. Countermeasures that preserve hepatic insulin sensitivity may represent a therapeutic target that could improve surgical outcomes in both diabetic and healthy patients.</p></div

Effects of anesthesia and diet on measures of glucose metabolism.

<p>Rd (A and B) and EGP (C and D) were assessed under conscious (black bars) and anesthetized (white bars) conditions in lean and fat fed animals (mean±SEM). Assessments were taken under low insulin (BASAL) conditions (A and C), and under the hyperinsulinemia induced by the CLAMP (B and D).</p

Insulin sensitivity with and without anesthesia.

<p>(A) Peripheral and (B) hepatic insulin sensitivity, as calculated from Rd and EGP, respectively was assessed under conscious (black bars) and anesthetized (white bars) conditions in lean and fat-fed animals (mean ± SEM).</p

Impact of sleep deprivation and high-fat feeding on insulin sensitivity and beta cell function in dogs

AIMS/HYPOTHESIS: Insufficient sleep is increasingly recognised as a major risk factor for the development of obesity and diabetes, and short-term sleep loss in clinical studies leads to a reduction in insulin sensitivity. Sleep loss-induced metabolic impairments are clinically relevant, since reductions in insulin sensitivity after sleep loss are comparable to insulin sensitivity differences between healthy individuals and those with impaired glucose tolerance. However, the relative effects of sleep loss vs high-fat feeding in the same individual have not been assessed. In addition, to our knowledge no diurnal (active during the daytime) non-human mammalian model of sleep loss-induced metabolic impairment exists, which limits our ability to study links between sleep and metabolism. METHODS: This study examined the effects of one night of total sleep deprivation on insulin sensitivity and beta cell function, as assessed by an IVGTT, before and after 9 months of high-fat feeding in a canine model. RESULTS: One night of total sleep deprivation in lean dogs impaired insulin sensitivity to a similar degree as a chronic high-fat diet (HFD)(normal sleep: 4.95 ± 0.45 mU-1 l-1 min-1; sleep deprivation: 3.14 ± 0.21 mU-1 l-1 min-1; HFD: 3.74 ± 0.48 mU-1 l-1 min-1; mean ± SEM). Hyperinsulinaemic compensation was induced by the chronic HFD, suggesting adequate beta cell response to high-fat feeding. In contrast, there was no beta cell compensation after one night of sleep deprivation, suggesting that there was metabolic dysregulation with acute sleep loss that, if sustained during chronic sleep loss, could contribute to the risk of type 2 diabetes. After chronic high-fat feeding, acute total sleep deprivation did not cause further impairments in insulin sensitivity (sleep deprivation + chronic HFD: 3.28 mU-1 l-1 min-1). CONCLUSIONS/INTERPRETATION: Our findings provide further evidence that sleep is important for metabolic health and establish a diurnal animal model of metabolic disruption during insufficient sleep

Later Meal and Sleep Timing Predicts Higher Percent Body Fat

Accumulating evidence suggests that later timing of energy intake (EI) is associated with increased risk of obesity. In this study, 83 individuals with overweight and obesity underwent assessment of a 7-day period of data collection, including measures of body weight and body composition (DXA) and 24-h measures of EI (photographic food records), sleep (actigraphy), and physical activity (PA, activity monitors) for 7 days. Relationships between body mass index (BMI) and percent body fat (DXA) with meal timing, sleep, and PA were examined. For every 1 h later start of eating, there was a 1.25 (95% CI: 0.60, 1.91) unit increase in percent body fat (False Discovery Rate (FDR) adjusted p value = 0.010). For every 1 h later midpoint of the eating window, there was a 1.35 (95% CI: 0.51, 2.19) unit increase in percent body fat (FDR p value = 0.029). For every 1 h increase in the end of the sleep period, there was a 1.64 (95% CI: 0.56, 2.72) unit increase in percent body fat (FDR p value = 0.044). Later meal and sleep timing were also associated with lower PA levels. In summary, later timing of EI and sleep are associated with higher body fat and lower levels of PA in people with overweight and obesity