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AMP-activated protein kinase and energy balance in breast cancer
Ecem Esencan,Hong Zhao,Robert T Chatterton,Serdar E Bulun,Xiaoming Zha,Yelda C Orhan
- , 2017,
Abstract: Cancer growth and metastasis depends on the availability of energy. Energy-sensing systems are critical in maintaining a balance between the energy supply and utilization of energy for tumor growth. A central regulator in this process is AMP-activated protein kinase (AMPK). In times of energy deficit, AMPK is allosterically modified by the binding of increased levels of AMP and ADP, making it a target of specific AMPK kinases (AMPKKs). AMPK signaling prompts cells to produce energy at the expense of growth and motility, opposing the actions of insulin and growth factors. Increasing AMPK activity may thus prevent the proliferation and metastasis of tumor cells. Activated AMPK also suppresses aromatase, which lowers estrogen formation and prevents breast cancer growth. Biguanides can be used to activate AMPK, but AMPK activity is modified by many different interacting factors; understanding these factors is important in order to control the abnormal growth processes that lead to breast cancer neoplasia. Fatty acids, estrogens, androgens, adipokines, and another energy sensor, sirtuin-1, alter the phosphorylation and activation of AMPK. Isoforms of AMPK differ among tissues and may serve specific functions. Targeting AMPK regulatory processes at points other than the upstream AMPKKs may provide additional approaches for prevention of breast cancer neoplasia, growth, and metastasis
Lower Serum Androstenedione Levels in Pre-Rheumatoid Arthritis versus Normal Control Women: Correlations with Lower Serum Cortisol Levels
Alfonse T. Masi,Kevin B. Elmore,Azeem A. Rehman,Robert T. Chatterton,Ned J. Goertzen,Jean C. Aldag
Autoimmune Diseases , 2013, DOI: 10.1155/2013/593493
Abstract: Serum adrenal androgens (AAs), including androstenedione (Δ4A) and dehydroepiandrosterone sulfate (DHEAS), have been reported to be lower in female rheumatoid arthritis (RA) patients with early disease. Few data are available on hormonal status of women before the onset of clinical rheumatoid arthritis (pre-RA). A broad baseline panel of serum adrenal and sex steroids was compared in 36 female pre-RA to 144 matched cohort control (CN) subjects to determine differences in their mean values and in patterns of hormonal correlations. Study subjects having lower versus higher baseline serum cortisol levels than the total group's mean value were also analyzed separately to investigate differences in their hormonal levels and correlational patterns. In total subjects, mean (±SE) Δ4A level (nmol/L) was lower ( ) in 28 pre-RA cases ( ) versus 108 CN ( ). The significant ( ) difference was restricted to 9 pre-RA versus 53？CN subjects having lower cortisol levels ( versus ？nmol/L, resp.). In total subjects, no significant difference was found between study subjects in their bivariate correlations of the hormonal panel variables, unlike results found in the subgroups stratified by lower versus higher cortisol levels. A subgroup of pre-RA females may have relative adrenal cortical insufficiency, as reflected by lower Δ4A, especially observed among those subjects with lower cortisol levels. 1. Introduction Relative insufficiency of adrenal glucocorticoid (GC) and androgenic-anabolic (AA) hormones has been suspected to increase the risk of developing rheumatoid arthritis (RA) and to contribute to its multifactorial neuroendocrine immune (NEI) pathogenesis [1–8]. The characteristic age- and sex-specific incidence patterns of RA support a possible constitutional deficiency of adrenal cortical or sex hormones in a subset of susceptible women. The female-to-male (F？:？M) risk ratio of persons developing RA is approximately 2？:？1 during the juvenile and older ages but is significantly increased to about 5？:？1 during the female reproductive years [9]. Of further note, risk of RA onset increases with age in adults, particularly among females. The preceding risk data imply that males have relative protection over females during all ages, but particularly in the younger and middle adult years [9]. A recent study indicated that early age at menopause (≤45 years) was associated with the subsequent risk of developing RA [10]. The hazard remained significant after adjusting for smoking, educational level, and length of breastfeeding [10]. Available data imply that the woman’s risk
Controlled Cohort Study of Serum Gonadal and Adrenocortical Steroid Levels in Males Prior to Onset of Rheumatoid Arthritis (pre-RA): A Comparison to pre-RA Females and Sex Differences among the Study Groups
Alfonse T. Masi,Azeem A. Rehman,Robert T. Chatterton,Huaping Wang,Ned J. Goertzen,Kevin B. Elmore,Jean C. Aldag
International Journal of Rheumatology , 2013, DOI: 10.1155/2013/284145
Abstract: Serum testosterone levels are generally reported to be lower in male rheumatoid arthritis (RA) patients, but it is not determined if a deficiency may occur before clinical onset of disease (pre-RA). Lower testosterone levels were recently reported in males many years before RA onset but were predictive only of rheumatoid factor (RF)—negative disease. A preceding prospective study did not reveal androgenic-anabolic hormone association with risk of RA in men or women. This cohort study of males analyzed baseline serum levels of gonadal and adrenocortical steroids, luteinizing hormone, and prolactin in 18 pre-RA versus 72 matched non-RA control (CN) subjects. Findings in males were compared to those in female pre-RA and CN subjects in the same cohort, and sex differences were analyzed. Steroidal and hormonal levels, including total testosterone, were similar between male study groups. In females, mean (±SE) serum androstenedione (nmol/L) was slightly ( ) lower in 36 pre-RA (6.7 ± 0.36) than 144 CN (7.6 ± 0.22). With the exception of 3 partial correlations of hormonal variables observed to differ between pre-RA versus CN subjects, the patterns were similar overall. However, partial correlations of hormonal variables differed frequently by sex, both within and between study groups. 1. Introduction The onset of rheumatoid arthritis (RA) occurs about 5-fold more frequently in women of child-bearing ages than among male counterparts [1]. Early age at menopause (≤45？yrs) was recently found to be associated with the subsequent risk of developing RA [2]. Such findings suggest that sex hormones may influence predisposition to this disease in women. In male RA patients with active disease, testosterone levels are reported to be lower than those in healthy control (CN) subjects [3, 4]. However, it is not known if such hormonal alteration results from inflammatory manifestations of active clinical disease or if it may be a preexisting risk factor before clinical onset (pre-RA). Recently, testosterone levels were reported to be lower in males many years before RA onset, as identified in a large Swedish cohort [5]. However, a significant association of lower testosterone levels was predictive only for the minority subset of patients having negative rheumatoid factor (RF-negative) disease [5]. A preceding retrospective case-control nested study within a large Finnish cohort did not find baseline serum total testosterone or dehydroepiandrosterone sulfate (DHEAS) levels to be predictive of the subsequent onset of RA, either in 32-male or in 84-female cases [6]. Our
Childhood Conditions Influence Adult Progesterone Levels
Alejandra Nú？ez-de la Mora ,Robert T Chatterton,Osul A Choudhury,Dora A Napolitano,Gillian R Bentley
PLOS Medicine , 2007, DOI: 10.1371/journal.pmed.0040167
Abstract: Background Average profiles of salivary progesterone in women vary significantly at the inter- and intrapopulation level as a function of age and acute energetic conditions related to energy intake, energy expenditure, or a combination of both. In addition to acute stressors, baseline progesterone levels differ among populations. The causes of such chronic differences are not well understood, but it has been hypothesised that they may result from varying tempos of growth and maturation and, by implication, from diverse environmental conditions encountered during childhood and adolescence. Methods and Findings To test this hypothesis, we conducted a migrant study among first- and second-generation Bangladeshi women aged 19–39 who migrated to London, UK at different points in the life-course, women still resident in Bangladesh, and women of European descent living in neighbourhoods similar to those of the migrants in London (total n = 227). Data collected included saliva samples for radioimmunoassay of progesterone, anthropometrics, and information from questionnaires on diet, lifestyle, and health. Results from multiple linear regression, controlled for anthropometric and reproductive variables, show that women who spend their childhood in conditions of low energy expenditure, stable energy intake, good sanitation, low immune challenges, and good health care in the UK have up to 103% higher levels of salivary progesterone and an earlier maturation than women who develop in less optimal conditions in Sylhet, Bangladesh (F9,178 = 5.05, p < 0.001, standard error of the mean = 0.32; adjusted R2 = 0.16). Our results point to the period prior to puberty as a sensitive phase when changes in environmental conditions positively impact developmental tempos such as menarcheal age (F2,81 = 3.21, p = 0.03) and patterns of ovarian function as measured using salivary progesterone (F2,81 = 3.14, p = 0.04). Conclusions This research demonstrates that human females use an extended period of the life cycle prior to reproductive maturation to monitor their environment and to modulate reproductive steroid levels in accordance with projected conditions they might encounter as adults. Given the prolonged investment of human pregnancy and lactation, such plasticity (extending beyond any intrauterine programming) enables a more flexible and finely tuned adjustment to the potential constraints or opportunities of the later adult environment. This research is the first, to our knowledge, to demonstrate a postuterine developmental component to variation in reproductive steroid
Glucose absorption and gastric emptying in critical illness
Marianne J Chapman, Robert JL Fraser, Geoffrey Matthews, Antonietta Russo, Max Bellon, Laura K Besanko, Karen L Jones, Ross Butler, Barry Chatterton, Michael Horowitz
Critical Care , 2009, DOI: 10.1186/cc8021
Abstract: Studies were performed in nineteen mechanically-ventilated critically ill patients and compared to nineteen healthy subjects. Following 4 hours fasting, 100 ml of Ensure, 2 g 3-O-methyl glucose (3-OMG) and 99mTc sulphur colloid were infused into the stomach over 5 minutes. Glucose absorption (plasma 3-OMG), blood glucose levels and GE (scintigraphy) were measured over four hours. Data are mean ± SEM. A P-value < 0.05 was considered significant.Absorption of 3-OMG was markedly reduced in patients (AUC240: 26.2 ± 18.4 vs. 66.6 ± 16.8; P < 0.001; peak: 0.17 ± 0.12 vs. 0.37 ± 0.098 mMol/l; P < 0.001; time to peak; 151 ± 84 vs. 89 ± 33 minutes; P = 0.007); and both the baseline (8.0 ± 2.1 vs. 5.6 ± 0.23 mMol/l; P < 0.001) and peak (10.0 ± 2.2 vs. 7.7 ± 0.2 mMol/l; P < 0.001) blood glucose levels were higher in patients; compared to healthy subjects. In patients; 3-OMG absorption was directly related to GE (AUC240; r = -0.77 to -0.87; P < 0.001; peak concentrations; r = -0.75 to -0.81; P = 0.001; time to peak; r = 0.89-0.94; P < 0.001); but when GE was normal (percent retention240 < 10%; n = 9) absorption was still impaired. GE was inversely related to baseline blood glucose, such that elevated levels were associated with slower GE (ret 60, 180 and 240 minutes: r > 0.51; P < 0.05).In critically ill patients; (i) the rate and extent of glucose absorption are markedly reduced; (ii) GE is a major determinant of the rate of absorption, but does not fully account for the extent of impaired absorption; (iii) blood glucose concentration could be one of a number of factors affecting GE.Delayed gastric emptying (GE) occurs frequently in critically ill patients [1] and is associated with impaired tolerance to naso-gastric feeding [2]. By slowing the transfer of food from the stomach into the small intestine and, thereby, reducing or delaying exposure of nutrient to small bowel mucosa, gastric stasis has the potential to adversely affect both the rate and extent of nutrient absorpti
Polychlorinated biphenyl exposure, diabetes and endogenous hormones: a cross-sectional study in men previously employed at a capacitor manufacturing plant
Victoria Persky, Julie Piorkowski, Mary Turyk, Sally Freels, Robert Chatterton, John Dimos, H Bradlow, Lin Chary, Virlyn Burse, Terry Unterman, Daniel W Sepkovic, Kenneth McCann
Environmental Health , 2012, DOI: 10.1186/1476-069x-11-57
Abstract: This paper examines associations of PCBs with diabetes and endogenous hormones in 63 men previously employed at the same plant who in 1996 underwent surveys of their exposure and medical history and collection of bloods and urine for measurements of PCBs, lipids, liver function, hematologic markers and endogenous hormones.PCB exposure was positively associated with diabetes and age and inversely associated with thyroid stimulating hormone and triiodothyronine-uptake. History of diabetes was significantly related to total PCBs and all PCB functional groupings, but not to quarters worked and job score, after control for potential confounders. None of the exposures were related to insulin resistance (HOMA-IR) in non-diabetic men.Associations of PCBs with specific endogenous hormones differ in some respects from previous findings in postmenopausal women employed at the capacitor plant. Results from this study, however, do confirm previous reports relating PCB exposure to diabetes and suggest that these associations are not mediated by measured endogenous hormones.Polychlorinated biphenyls (PCBs) are a form of organochlorines that are very stable and resistant to temperature and pressure extremes. They were first commercially produced in the United States in 1929 and used widely in capacitors, transformers, hydraulic fluids, heat transfer fluids, lubricants, plasticizers and as components of surface coatings and ink until the USEPA banned its use in 1979. Employees at plants that used PCBs, such as capacitor manufacturing plants, were highly exposed with elevated levels that persist years after their employment [1]. In addition, PCBs are still present in many capacitors, transformers and other equipment manufactured before 1979, thus serving as a continuing source of indirect exposure for the general population, primarily through ingestion of contaminated food [2].This paper focuses on associations of exposure to PCBs through previous employment at a capacitor manufactur
The prevalence and genotypic analysis of Toxoplasma gondii from individuals in Scotland, 2006–2012
Alison Burrells,Chris-Anne McKenzie,Claire L. Alexander,Dolores Hill,Elisabeth A. Innes,Frank Katzer,Jean Chatterton,Kevin G. Pollock,Marieke Opsteegh,Robert Walker,Roger Evans
- , 2016, DOI: 10.1186/s13071-016-1610-6
Abstract: Contemporary information relating to the prevalence of Toxoplasma gondii in humans is lacking for the UK population, with even less information available about the human prevalence of the parasite in Scotland. To address this, two different study groups were used to determine the prevalence and genotypes of Toxoplasma gondii in the Scottish population
Examination of Duct Physiology in the Human Mammary Gland
Ameer Gomberawalla,Dixie Mills,Eva J. Gordon,Janice M. Pogoda,Jianyu Rao,Julie Tondre,Mitra Nejad,Robert Chatterton,Susan M. Love,Susanne Henning,Tinh Nguyen
- , 2016, DOI: 10.1371/journal.pone.0150653
Abstract:
Gastric emptying is slow in chronic fatigue syndrome
Richard B Burnet, Barry E Chatterton
BMC Gastroenterology , 2004, DOI: 10.1186/1471-230x-4-32
Abstract: Thirty-two (32) patients with CFS and 45 control subjects completed a questionnaire on upper GI symptoms, and the 32 patients underwent oesophageal clearance, and simultaneous liquid and solid gastric emptying studies using radionuclide techniques compared with historical controls.The questionnaires showed a significant difference in gastric (p > 0.01) symptoms and swallowing difficulty. Nocturnal diarrhoea was a significant symptom not previously reported.5/32 CFS subjects showed slightly delayed oesophageal clearance, but overall there was no significant difference from the control subjects, nor correlation of oesophageal clearance with symptoms. 23/32 patients showed a delay in liquid gastric emptying, and 12/32 a delay in solid gastric emptying with the delay significantly correlated with the mean symptom score (for each p ？ 0.001).GI symptoms in patients with chronic fatigue syndrome are associated with objective changes of upper GI motility.Chronic Fatigue Syndrome (CFS) is a descriptive term used to define a classifiable pattern of symptoms that cannot be attributed to any alternative condition [1]. It can be associated with immunological alterations, neuro-endocrine changes [2], sleep disturbance and disturbed neurocognitive performance with abnormal cerebral perfusion [3], but the pathophysiological significance of these is uncertain. Skeletal neuromuscular function is usually normal in CFS sufferers [4].Many with CFS have gastro-intestinal (GI) symptoms, which are often unrecognised as being part of CFS. The commonest of the upper GI symptoms include fullness and bloating after a small meal, abdominal distension, nausea, and loss of appetite. Lower GI tract symptoms have considerable overlap with irritable bowel syndrome [5].The hypothesis explored in this paper is that symptoms of possible upper gastrointestinal origin are more common in patients with CFS and are related to upper gastrointestinal motility as assessed by radionuclide methods.Consecutive pa
Fish Consumption Advisories and the Surprising Relationship to Prevalence Rate of Developmental Disability as Reported by Public Schools  [PDF]
M. Catherine DeSoto, Robert T. Hitlan
Journal of Environmental Protection (JEP) , 2012, DOI: 10.4236/jep.2012.311174
Abstract: According to the Environmental Protection Agency (EPA), fish consumption is the most significant route of mercury exposure, and the concern is greatest for women of childbearing age due to the potential for neurodevelopmental effects on a developing fetus. Rates of developmental disorders vary. But in 2008 it was demonstrated that the rate of autism is higher near industries that emit heavy metals. Furthermore past research findings can be taken to show that where a pregnancy occurred may predict later autism likelihood in the offspring more than where diagnosis occurs. If mercury plays any role in developmental disabilities, the rate of disability should relate to any reliable direct measure of contamination. The current research focuses on one index of environmental mercury contamination. Specifically, mercury-related fish advisories are found to be a surprisingly strong predictor of a state’s autism rate, r = 0.48, p < 0.001. The relationship remains strong after controlling for student to teacher ratio and per pupil spending. It is argued that a secular increase in autism has been occurring and that prenatal exposure to heavy metal toxins may play a significant role. Because we suspect this finding may be of some interest, the full data set is provided in the appendix so that researchers can independently analyze the key findings which rely on CDC, EPA and IDEA data sets.
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