The Experts below are selected from a list of 360 Experts worldwide ranked by ideXlab platform
G R Oetzel - One of the best experts on this subject based on the ideXlab platform.
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monitoring and testing dairy herds for Metabolic Disease
Veterinary Clinics of North America-food Animal Practice, 2004Co-Authors: G R OetzelAbstract:Metabolic Disease incidence typically increases as milk production increases and as herds become larger. These factors favor the use of rigorous, quantitative monitoring of Metabolic Disease whenever possible. Fortunately, recent developments of herd-based tests plus new applications of some old tests are now available for use in routine herd monitoring and for investigating dairy herds with Metabolic Disease problems. This allows the herd consultant to make recommendations based on objective data rather than subjective impressions alone. This article will focus on strategies for testing and monitoring subacute ruminal acidosis (SARA), subclinical ketosis (SCK), and parturient hypocalcemia (clinical plus subclinical milk fever) in dairy herds. Quantitative data about these Diseases have been published, and are the foundation for their use and interpretation on a herd basis. Additionally, these three disorders are gateway conditions for other Metabolic disorders such as laminitis, displaced abomasum, impaired immune function, retained placenta, and cystic ovarian Disease. Other Metabolic Diseases can be important problems in dairies (eg, hypomagnesemia, udder edema, hypokalemia, and so on), but these are less common disorders with limited published data.
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monitoring and testing dairy herds for Metabolic Disease
Veterinary Clinics of North America-food Animal Practice, 2004Co-Authors: G R OetzelAbstract:Clinical impressions of Metabolic Disease problems in dairy herds can be corroborated with herd-based Metabolic testing. Ruminal pH should be evaluated in herds showing clinical signs associated with SARA (lame cows, thin cows, high herd removals or death loss across all stages of lactation, or milk fat depression). Testing a herd for the prevalence of SCK via blood BHB sampling in early lactation is useful in almost any dairy herd, and particularly if the herd is experiencing a high incidence of displaced abomasum or high removal rates of early lactation cows. If cows are experiencing SCK within the first 3 weeks of lactation, then consider NEFA testing of the prefresh cows to corroborate prefresh negative energy balance. Finally, monitoring cows on the day of calving for parturient hypocalcemia can provide early detection of diet-induced problems in calcium homeostasis. If hypocalcemia problems are present despite supplementing anionic salts before calving, then it may be helpful to evaluate mean urinary pH of a group of the prefresh cows. Quantitative testing strategies based on statistical analyses can be used to establish minimum sample sizes and interpretation guidelines for all of these tests.
Kenneth P Wright - One of the best experts on this subject based on the ideXlab platform.
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the shift work and health research agenda considering changes in gut microbiota as a pathway linking shift work sleep loss and circadian misalignment and Metabolic Disease
Sleep Medicine Reviews, 2017Co-Authors: Amy C Reynolds, Jessica L Paterson, Sally A Ferguson, Dragana Stanley, Kenneth P Wright, Drew DawsonAbstract:Prevalence and impact of Metabolic Disease is rising. In particular, overweight and obesity are at epidemic levels and are a leading health concern in the Western world. Shift work increases the risk of overweight and obesity, along with a number of additional Metabolic Diseases, including Metabolic syndrome and type 2 diabetes (T2D). How shift work contributes to Metabolic Disease has not been fully elucidated. Short sleep duration is associated with Metabolic Disease and shift workers typically have shorter sleep durations. Short sleep durations have been shown to elicit a physiological stress response, and both physiological and psychological stress disrupt the healthy functioning of the intestinal gut microbiota. Recent findings have shown altered intestinal microbial communities and dysbiosis of the gut microbiota in circadian disrupted mice and jet lagged humans. We hypothesize that sleep and circadian disruption in humans alters the gut microbiota, contributing to an inflammatory state and Metabolic Disease associated with shift work. A research agenda for exploring the relationship between insufficient sleep, circadian misalignment and the gut microbiota is provided.
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role of sleep and circadian disruption on energy expenditure and in Metabolic predisposition to human obesity and Metabolic Disease
Obesity Reviews, 2017Co-Authors: Andrew W Mchill, Kenneth P WrightAbstract:Summary Weight gain, obesity and diabetes have reached alarming levels in the developed world. Traditional risk factors such as over-eating, poor nutritional choices and lack of exercise cannot fully account for the high prevalence of Metabolic Disease. This review paper examines the scientific evidence on two novel risk factors that contribute to dys-regulated Metabolic physiology: sleep disruption and circadian misalignment. Specifically, fundamental relationships between energy metabolism and sleep and circadian rhythms and the impact of sleep and circadian disruption on Metabolic physiology are examined. Millions of individuals worldwide do not obtain sufficient sleep for healthy Metabolic function, and many participate in shift work and social activities at times when the internal physiological clock is promoting sleep. These behaviours predispose an individual for poor Metabolic health by promoting excess caloric intake in response to reduced sleep, food intake at internal biological times when Metabolic physiology is not prepared, decreased energy expenditure when wakefulness and sleep are initiated at incorrect internal biological times, and disrupted glucose metabolism during short sleep and circadian misalignment. In addition to the traditional risk factors of poor diet and exercise, disturbed sleep and circadian rhythms represent modifiable risk factors for prevention and treatment of Metabolic Disease and for promotion of healthy metabolism.
Scott A Summers - One of the best experts on this subject based on the ideXlab platform.
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essential nutrient supplementation prevents heritable Metabolic Disease in multigenerational intrauterine growth restricted rats
The FASEB Journal, 2015Co-Authors: Danielle Goodspeed, Maxim Seferovic, William L Holland, Robert A Mcknight, Scott A Summers, Ware D Branch, Robert H Lane, Kjersti AagaardAbstract:Intrauterine growth restriction (IUGR) confers heritable alterations in DNA methylation, rendering risk of adult Metabolic syndrome (MetS). Because CpG methylation is coupled to intake of essential nutrients along the one-carbon pathway, we reasoned that essential nutrient supplementation (ENS) may abrogate IUGR-conferred multigenerational MetS. Pregnant Sprague-Dawley rats underwent bilateral uterine artery ligation causing IUGR in F1. Among the F2 generation, IUGR lineage rats were underweight at birth (6.7 vs. 8.0 g, P 30% elevated, P 5-fold less central fat mass, normal hepatic glucose efflux, and >70% reduced circulating triglycerides and very-LDLs compared with IUGR control-fed F2 offspring (P < 0.01). Moreover, increased methylation of the IGF-1 P2 transcriptional start site among IUGR lineage F2 offspring was reversed in ENS (P < 0.04). This is an initial demonstration that supplementation along the one-carbon pathway abrogates adult morbidity and associated epigenomic modifications of IGF-1 in a rodent model of multigenerational MetS.—Goodspeed, D., Seferovic, M. D., Holland, W., Mcknight, R. A., Summers, S. A., Branch, D. W., Lane, R. H., Aagaard, K. M. Essential nutrient supplementation prevents heritable Metabolic Disease in multigenerational intrauterine growth-restricted rats.
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sphingolipids insulin resistance and Metabolic Disease new insights from in vivo manipulation of sphingolipid metabolism
Endocrine Reviews, 2008Co-Authors: William L Holland, Scott A SummersAbstract:Obesity and dyslipidemia are risk factors for Metabolic disorders including diabetes and cardiovascular Disease. Sphingolipids such as ceramide and glucosylceramides, while being a relatively minor component of the lipid milieu in most tissues, may be among the most pathogenic lipids in the onset of the sequelae associated with excess adiposity. Circulating factors associated with obesity (e.g., saturated fatty acids, inflammatory cytokines) selectively induce enzymes that promote sphingolipid synthesis, and lipidomic profiling reveals relationships between tissue sphingolipid levels and certain Metabolic Diseases. Moreover, studies in cultured cells and isolated tissues implicate sphingolipids in certain cellular events associated with diabetes and cardiovascular Disease, including insulin resistance, pancreatic β-cell failure, cardiomyopathy, and vascular dysfunction. However, definitive evidence that sphingolipids contribute to insulin resistance, diabetes, and atherosclerosis has come only recently, as researchers have found that pharmacological inhibition or genetic ablation of enzymes controlling sphingolipid synthesis in rodents ameliorates each of these conditions. Herein we will review the role of ceramide and other sphingolipid metabolites in insulin resistance, β-cell failure, cardiomyopathy, and vascular dysfunction, focusing on these in vivo studies that identify enzymes controlling sphingolipid metabolism as therapeutic targets for combating Metabolic Disease.
Drew Dawson - One of the best experts on this subject based on the ideXlab platform.
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the shift work and health research agenda considering changes in gut microbiota as a pathway linking shift work sleep loss and circadian misalignment and Metabolic Disease
Sleep Medicine Reviews, 2017Co-Authors: Amy C Reynolds, Jessica L Paterson, Sally A Ferguson, Dragana Stanley, Kenneth P Wright, Drew DawsonAbstract:Prevalence and impact of Metabolic Disease is rising. In particular, overweight and obesity are at epidemic levels and are a leading health concern in the Western world. Shift work increases the risk of overweight and obesity, along with a number of additional Metabolic Diseases, including Metabolic syndrome and type 2 diabetes (T2D). How shift work contributes to Metabolic Disease has not been fully elucidated. Short sleep duration is associated with Metabolic Disease and shift workers typically have shorter sleep durations. Short sleep durations have been shown to elicit a physiological stress response, and both physiological and psychological stress disrupt the healthy functioning of the intestinal gut microbiota. Recent findings have shown altered intestinal microbial communities and dysbiosis of the gut microbiota in circadian disrupted mice and jet lagged humans. We hypothesize that sleep and circadian disruption in humans alters the gut microbiota, contributing to an inflammatory state and Metabolic Disease associated with shift work. A research agenda for exploring the relationship between insufficient sleep, circadian misalignment and the gut microbiota is provided.
Alon Chen - One of the best experts on this subject based on the ideXlab platform.
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sex dependent impact of gestational stress on predisposition to eating disorders and Metabolic Disease
Molecular metabolism, 2018Co-Authors: Mariana Schroeder, Mira Jakovcevski, Tamar Polacheck, Yonat Drori, Shifra Bendor, Alon ChenAbstract:Abstract Objective Vulnerability to eating disorders (EDs) is broadly assumed to be associated with early life stress. However, a careful examination of the literature shows that susceptibility to EDs may depend on the type, severity and timing of the stressor and the sex of the individual. We aimed at exploring the link between chronic prenatal stress and predisposition to EDs and Metabolic Disease. Methods We used a chronic variable stress protocol during gestation to explore the Metabolic response of male and female offspring to food restriction (FR), activity-based anorexia (ABA), binge eating (BE) and exposure to high fat (HF) diet. Results Contrary to controls, prenatally stressed (PNS) female offspring showed resistance to ABA and BE and displayed a lower Metabolic rate leading to hyperadiposity and obesity on HF diet. Male PNS offspring showed healthy responses to FR and ABA, increased propensity to binge and improved coping with HF compared to controls. We found that long-lasting abnormal responses to Metabolic challenge are linked to fetal programming and adult hypothalamic dysregulation in PNS females, resulting from sexually dimorphic adaptations in placental methylation and gene expression. Conclusions Our results show that maternal stress may have variable and even opposing effects on ED risk, depending on the ED and the sex of the offspring.