Metabolically Favorable Remodeling of Human Adipose Tissue by Human Adenovirus Type 36

Rogers, Pamela M.; Mashtalir, Nazar; Rathod, Miloni; Dubuisson, Olga; Wang, Zhong; Dasuri, Kumar; Babin, Scott; Gupta, Alok; Markward, Nathan; Cefalu, William T.; Dhurandhar, Nikhil V.

doi:10.2337/db07-1311

Cited by 71 publications

(82 citation statements)

References 71 publications

(80 reference statements)

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“…Adipocyte remodeling has been observed in response to the peroxisome proliferator-activated receptor gamma agonist thiazolidinedione 79 and benzopyran-derived T33, 80 but also human adenovirus type 36. 81,82 Animal studies have…”

Section: Future Studies and Potential Mechanismsmentioning

confidence: 99%

Characterizing the profile of obese patients who are metabolically healthy

et al. 2010

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The presence of obesity-related metabolic disturbances varies widely among obese individuals. Accordingly, a unique subset of obese individuals has been described in the medical literature, which seems to be protected or more resistant to the development of metabolic abnormalities associated with obesity. These individuals, now known as 'metabolically healthy but obese' (MHO), despite having excessive body fatness, display a favorable metabolic profile characterized by high levels of insulin sensitivity, no hypertension as well as a favorable lipid, inflammation, hormonal, liver enzyme and immune profile. However, recent studies have indicated that this healthier metabolic profile may not translate into a lower risk for mortality. Mechanisms that could explain the favorable metabolic profile of MHO individuals are poorly understood. However, preliminary evidence suggests that differences in visceral fat accumulation, birth weight, adipose cell size and gene expression-encoding markers of adipose cell differentiation may favor the development of the MHO phenotype. Despite the uncertainty regarding the exact degree of protection related to the MHO status, identification of underlying factors and mechanisms associated with this phenotype will eventually be invaluable in helping us understand factors that predispose, delay or protect obese individuals from metabolic disturbances. Collectively, a greater understanding of the MHO individual has important implications for therapeutic decision making, the characterization of subjects in research protocols and medical education. Keywords: metabolically healthy but obese; insulin sensitivity; body composition; metabolic risk factors; cardiovascular diseases Introduction Obesity has been increasing at a rapid rate over the past decades and has now reached epidemic proportions. Recent data suggest that 65% of US adult are overweight (body mass index425 kg m À2) and 30% are obese (body mass index430 kg m À2).1 Obesity is associated with numerous metabolic complications such as Type 2 diabetes, dyslipidemia, hypertension, cardiovascular diseases and several forms of cancer. 2 The risk of developing obesity-related complications is proportional to the degree of obesity, and more specifically to android fat accumulation. 3 However, the presence of these obesity-related metabolic disturbances varies widely among obese individuals. 4,5 Accordingly, a unique subset of obese individuals has been described in the medical literature that seems to be protected or more resistant to the development of metabolic abnormalities associated with obesity. 6-12 These individuals, now known as 'metabolically healthy but obese' (MHO), despite having excessive body fatness, display favorable metabolic profiles characterized by high levels of insulin sensitivity, no hypertension, as well as favorable lipid, inflammation, hormonal, liver enzyme and immune profiles 7,9,[13][14][15] ( Figure 1). This phenomenon has also been observed in adolescents. 16 Despite a clinical awareness of the MHO individu...

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Section: Future Studies and Potential Mechanismsmentioning

confidence: 99%

Characterizing the profile of obese patients who are metabolically healthy

et al. 2010

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“…In these studies, the absence of unfavourable functions of Ad36 infection on insulin sensitivity was reported, even in the presence of adipogenic-associated effects. 15 Overweight and obese patients, without other associated conditions, such as diabetes, show regularly increased circulating levels of insulin and other signs of decreased insulin sensitivity. 20,21 However, obesity is a complex Obesity, Ad36 and insulin resistance GM Trovato et al condition with many causal contributors, including genetic ones and environmental factors; these last are largely beyond individuals' abilities to choose or control.…”

Section: Obesity Ad36 and Insulin Resistance Gm Trovato Et Almentioning

confidence: 99%

“…The mechanisms involved appear to lead to expansion of adipose tissue and increase of glucose uptake in skeletal muscle and adipose tissue, which collectively might lead to better glycemic control in vivo. 15 Increased body weight (BW) is a relevant factor for many diseases, including essential hypertension, whose relationship with obesity is indicated by the increase of some dimensions, and especially body mass index (BMI), waisthip ratio (WHR), and relative body composition, which, assessed by bio-impedance assessment (BIA), can provide detailed information on body compartments. 13 Little information on the relationship, if any, of adenoviruses seropositivity with circulating insulin, IR, and body composition is presently available.…”

Section: Introductionmentioning

confidence: 99%

Human obesity relationship with Ad36 adenovirus and insulin resistance

et al. 2009

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Objectives: Infection with specific pathogens may lead to increased adiposity: a specific adiposity-promoting effect of Ad36 human adenovirus, without the involvement of neurological mechanisms, was reported. The aim of this study is to investigate whether non-diabetic patients with earlier Ad36 infection show greater degrees of overweight obesity, of Insulin Resistance (IR), assessed by homoeostasis-model assessment (HOMA), and/or of other related factors. Moreover, the relationship, if any, among these factors and an earlier Ad36 infection, and the hypothesis of a mechanism involving IR are investigated. Subjects: Ad36 seropositivity is assessed in 68 obese and 135 non-obese subjects, along with body composition, HOMA and laboratory investigations. Results: Age, body mass index (BMI), waist-hip ratio, blood pressure, insulin, HOMA and triglycerides are significantly greater in the Ad36 seropositive group. Ad36 seropositivity, along with HOMA and total cholesterol, explains BMI variance. No Ad36 seropositivity effect to HOMA could be envisaged by the same statistical model. Conclusion: A significant association of Ad36 seropositivity with obesity and with essential hypertension in human beings is suggested by our study; this association is mostly significant in women. Our results do not support that any Ad36 adipogenic adenovirus effect is operating in human obesity through an insulin-resistance-related mechanism. Ad36 seropositive status could also be a hallmark of a clinical-metabolic profile possibly preceding obesity and diabetes in non-obese patients.

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“…A separate cohort of female offspring born to sedentary and exercise dams was fasted for 3 h at 36 wk of age (n ϭ 4/group). Glucose uptake was performed as described previously with some modifications (37). Briefly, parametrial fat was removed immediately after euthanasia and cut into 5-to 10-mg sized explants.…”

Section: Animals and Dietsmentioning

confidence: 99%

Perinatal exercise improves glucose homeostasis in adult offspring

Carter

Lewis

Wilkerson

et al. 2012

American Journal of Physiology-Endocrinology and Metabolism

138

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Emerging research has shown that subtle factors during pregnancy and gestation can influence long-term health in offspring. In an attempt to be proactive, we set out to explore whether a nonpharmacological intervention, perinatal exercise, might improve offspring health. Female mice were separated into sedentary or exercise cohorts, with the exercise cohort having voluntary access to a running wheel prior to mating and during pregnancy and nursing. Offspring were weaned, and analyses were performed on the mature offspring that did not have access to running wheels during any portion of their lives. Perinatal exercise caused improved glucose disposal following an oral glucose challenge in both female and male adult offspring (P Ͻ 0.05 for both). Blood glucose concentrations were reduced to lower values in response to an intraperitoneal insulin tolerance test for both female and male adult offspring of parents with access to running wheels (P Ͻ 0.05 and P Ͻ 0.01, respectively). Male offspring from exercised dams showed increased percent lean mass and decreased fat mass percent compared with male offspring from sedentary dams (P Ͻ 0.01 for both), but these parameters were unchanged in female offspring. These data suggest that short-term maternal voluntary exercise prior to and during healthy pregnancy and nursing can enhance long-term glucose homeostasis in offspring.running; pregnancy; programming; mice IN 2007, 23.5 MILLION PEOPLE in the US were estimated to have diabetes, and this number is increasing (4). Interestingly, and what is often underappreciated, is that the metabolic status of an individual is decided not only by their inherited genes, nutritional intake, and physical exercise but also by maternal nutrition and obesity during pregnancy. In 1992, Hales and Barker (18) put forth the thrifty phenotype hypothesis that suggested that malnourished pregnant mothers produce smaller offspring that have a higher incidence of obesity, diabetes, and heart disease in adulthood. This hypothesis has since been modified to the developmental origins of health and disease (DOHaD) (15,17,18).The DOHaD suggests that the maternal environment and fetal programming lead to a higher incidence of several diseases later in life (14, 16). A growing number of studies have been designed to provide evidence for the negative impact of DOHaD, using mice, rats, and sheep as animal models (11,12,31,38). Many of these studies are directed at malnutrition through protein restriction or physical stressors that produce similar effects (8,11,34,44,45), but more recent studies are elucidating the metabolic effects of high-fat diet consumption during pregnancy on offspring (22,38,44,48).It has been known since Hippocrates and Galen that physical activity is an important component of a healthy lifestyle (33). However, knowledge about the contributions of maternal exercise during pregnancy and the long-term consequences on offspring is minimal. In both rats and mice, maternal exercise during pregnancy can improve brain physiology and cognition...

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Metabolically Favorable Remodeling of Human Adipose Tissue by Human Adenovirus Type 36

Cited by 71 publications

References 71 publications

Characterizing the profile of obese patients who are metabolically healthy

Characterizing the profile of obese patients who are metabolically healthy

Human obesity relationship with Ad36 adenovirus and insulin resistance

Perinatal exercise improves glucose homeostasis in adult offspring

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