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1.
Mechanistic Targets and Nutritionally Relevant Intervention Strategies to Break Obesity-Breast Cancer Links.
Bustamante-Marin, XM, Merlino, JL, Devericks, E, Carson, MS, Hursting, SD, Stewart, DA
Frontiers in endocrinology. 2021;:632284
Abstract
The worldwide prevalence of overweight and obesity has tripled since 1975. In the United States, the percentage of adults who are obese exceeds 42.5%. Individuals with obesity often display multiple metabolic perturbations, such as insulin resistance and persistent inflammation, which can suppress the immune system. These alterations in homeostatic mechanisms underlie the clinical parameters of metabolic syndrome, an established risk factor for many cancers, including breast cancer. Within the growth-promoting, proinflammatory milieu of the obese state, crosstalk between adipocytes, immune cells and breast epithelial cells occurs via obesity-associated hormones, angiogenic factors, cytokines, and other mediators that can enhance breast cancer risk and/or progression. This review synthesizes evidence on the biological mechanisms underlying obesity-breast cancer links, with emphasis on emerging mechanism-based interventions in the context of nutrition, using modifiable elements of diet alone or paired with physical activity, to reduce the burden of obesity on breast cancer.
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2.
Extra-Skeletal Effects of Vitamin D.
Bouillon, R
Frontiers of hormone research. 2018;:72-88
Abstract
There are very solid data to confirm that the vitamin D endocrine system is important not only for calcium transport or bone homeostasis but also for operational functions in most cells of the body. Preclinical studies convincingly demonstrated coherent actions of the vitamin D endocrine system on the proliferation/differentiation of most cells (and thus possibly on the evolution of cancer). The most plausible target tissues include skeletal and cardiac muscle, all immune cells, many cells involved in cardiovascular homeostasis, brain cells, and reproductive tissues. These data have been generated in models of (near) total absence of vitamin D action or when exposed to very high concentrations of the active hormone, 1,25-dihydroxyvitamin D or its analogs. In humans, observational data frequently demonstrate a link between poor vitamin D status and a large number of major human diseases such as cancer, muscle weakness and falls, infections or autoimmune diseases, hypertension and cardiovascular risks and events, obesity, diabetes and all aspects of the metabolic syndrome, and other health problems. Intervention studies so far have not convincingly demonstrated a positive effect on such extra-skeletal health outcomes. A very large number of ongoing studies (about 3,000), however, should help to clarify the role of vitamin D on the musculoskeletal system and on global health.
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3.
Diets link metabolic syndrome and colorectal cancer development (Review).
Saetang, J, Sangkhathat, S
Oncology reports. 2017;(3):1312-1320
Abstract
Diets have been believed to be an important factor in the development of metabolic syndrome and colorectal cancer (CRC). In recent years, many studies have shown an intimate relationship between mucosal immunity, metabolism and diets, which has led to a greater understanding of the pathophysiology of metabolic syndrome and CRC development. Although the precise effects of diets on oncogenesis have not been compl-etely elucidated, microbiota changes and inflammation are believed to be important factors that influence the development of CRC. Moreover, increased release of pro-inflammatory cytokines and alteration of adipokine levels have been observed in patients with colorectal adenoma and/or CRC, and these all have been considered as the important mechanisms that link diets to the development of metabolic syndrome and CRC. Importantly, a high-fat, low-fiber diet is associated with dysbiosis, and as the gut signature becomes more important in metabolic syndrome and CRC, an increased understanding of diets on bacterial activity in the pathogenesis of metabolic syndrome and CRC will lead to new preventive and therapeutic strategies.
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4.
Effect of an isoenergetic traditional Mediterranean diet on the high-density lipoprotein proteome in men with the metabolic syndrome.
Richard, C, Couture, P, Desroches, S, Nehmé, B, Bourassa, S, Droit, A, Lamarche, B
Journal of nutrigenetics and nutrigenomics. 2014;(1):48-60
Abstract
BACKGROUND/AIMS: The objective of this preliminary study was to examine the impact of the Mediterranean diet (MedDiet) on the high-density lipoprotein (HDL) proteome in men with the metabolic syndrome (MetS). METHODS Twenty-six men with the MetS first consumed a standardized baseline North American isoenergetic control diet (5 weeks) and then consumed an isoenergetic MedDiet (5 weeks), both in full feeding condition. The HDL fraction was isolated by ultracentrifugation at the end of each diet and the HDL proteome assessed by isobaric tags for relative and absolute quantitation and mass spectrometry. RESULTS Of all proteins identified within HDL, only 3 showed significant changes in relative abundance after the MedDiet versus the control diet, including a reduction in inflammation-related inter-α-trypsin inhibitor heavy chain H4 (fold change: 0.62) and hemoglobin subunits α (fold change: 0.40) and β (fold change: 0.46). Other HDL-bound proteins associated with functions related to lipid metabolism/cholesterol homeostasis, oxidation, coagulation, complement activation and immunity were unchanged after consumption of the MedDiet for 5 weeks. CONCLUSIONS Changes in the HDL proteome may explain, at least partly, the well-known anti-inflammatory effect ascribed to the MedDiet. Otherwise, short-term consumption of the MedDiet seems to have little impact on other features of the HDL proteome in men with the MetS.
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5.
Polyunsaturated fatty acids in pregnancy and metabolic syndrome: a review.
Poniedzialek-Czajkowska, E, Mierzynski, R, Kimber-Trojnar, Z, Leszczynska-Gorzelak, B, Oleszczuk, J
Current pharmaceutical biotechnology. 2014;(1):84-99
Abstract
This review presents available evidence for possible application of n-3 long chain polyunsaturated fatty acids (PUFAs) in pregnant obese women with metabolic syndrome (MS) and focuses on prophylaxis of pregnancy complications associated with MS such as gestational hypertension, preeclampsia and gestational diabetes. Dietary supplementation with n-3 PUFAs has recently become popular and their adequate intake during pregnancy and early childhood is of clinical importance. The results of experimental and epidemiological investigations reveal that n-3 PUFAs, especially α- linolenic acid (ALA), eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA), may decrease the risk of cardiovascular diseases. It is believed that n-3 PUFAs affect a multitude of molecular pathways, involving regulation of gene expression, alteration of physical and chemical properties of cellular membranes and modulation of membrane channels and proteins. A large body of evidence focuses on anti-inflammatory properties of PUFAs which seem to be fundamental in prevention and reversing of insulin resistance, atherogenic dyslipidemia, hypertension, thromboembolism and in improving vascular function. Despite the potential PUFAs benefits of decreasing insulin resistance, their application in order to prevent preeclampsia, gestational hypertension and gestational diabetes mellitus in pregnant women with MS has not yet been established. Numerous reports have revealed that appropriate fetal development, including neuronal, retinal and immune function depends on EPA and DHA which are crucial also for prevention of preterm birth. Thus the supplementation with EPA and DHA is highly recommended during pregnancy although the optimal dosing and treatment strategies still need to be determined.
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6.
[Evaluation of the relationships between plasma homocysteine level and selected low-grade inflammation indices according to the prevalence of metabolic syndrome in men].
Herman, WA, Krzoska, A, Łacka, K, Bugaj, R, Dorszewska, J
Polski merkuriusz lekarski : organ Polskiego Towarzystwa Lekarskiego. 2013;(204):320-4
Abstract
UNLABELLED Metabolic syndrome (MS) is associated with low-grade systemic inflammation. Hyperhomocysteinemia is considered recently as a consequence of immune activation. Acute phase proteins, proinflammatory cytokines and probably homocysteine (hHcy) are involved in the pathogenesis of MS, atherosclerosis and ageing. The aim of our study was to investigate the reciprocal links between hHcy and selected negative and positive acute phase reactants as well as interleukin-18 in men over 40 years of age suffering from MS compared to healthy subjects. MATERIAL AND METHODS In 160 randomly selected men aged 40 to 70 years hHcy, C-reactive protein, transferrin, alpha1-antichymotrypsin and IL-18 were evaluated and features of MS using IDF (International Diabetes Federation-2005) criteria were estimated. RESULTS Hcy plasma levels are not correlated with age. Men suffering from MS revealed significantly higher serum hHcy levels than healthy subjects (11.52 +/- 6.87 microM/L vs 10.08 +/- 5.44 microM/L, p = 0.0074). A weak but positive (r = 0.099; p = 0.014) correlation between hHcy and the numbers of MS traits is shown. However, the plasma hHcy level is correlated only with HDL-cholesterol serum levels (r = -0.132; p = 0.035) and fasting blood glucose (r = 0.164; p = 0.009). hHcy concentration is strongly positively correlated with IL-18 (r = 0.276; p = 0.005), although not with CRP, alpha1-ACT and transferrin. CONCLUSIONS In men over 40 years of age suffering from MS significant higher serum Hcy levels than healthy subjects are presented, but hHcy (as opposed to acute phase reactants) correlates only with IL-18 plasma concentrations.
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7.
Role of fatty acids and polyphenols in inflammatory gene transcription and their impact on obesity, metabolic syndrome and diabetes.
Sears, B, Ricordi, C
European review for medical and pharmacological sciences. 2012;(9):1137-54
Abstract
Obesity, metabolic syndrome and diabetes represent multi-factorial conditions resulting from improper balances of hormones and gene expression. In addition, these conditions have a strong inflammatory component that can potentially be impacted by the diet. The purpose of this review is to discuss the molecular targets that can be addressed by anti-inflammatory nutrition. These molecular targets range from reduction of pro-inflammatory eicosanoids that can alter hormonal signaling cascades to the modulation of the innate immune system, via toll-like receptors and gene transcription factors. Working knowledge of the impact of nutrients, especially dietary fatty acids and polyphenols, on these various molecular targets makes it possible to develop a general outline of an anti-inflammatory diet that offers a unique, non-pharmacological approach for treating obesity, metabolic syndrome and diabetes.
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8.
Developmental origins of the metabolic syndrome: body clocks and stress responses.
Cagampang, FR, Poore, KR, Hanson, MA
Brain, behavior, and immunity. 2011;(2):214-20
Abstract
The prevalence of the metabolic syndrome, which represents a spectrum of metabolic and cardiovascular disorders, continues to increase at an alarming rate in contemporary society. Inadequate responses of an individual to environmental challenges such as unbalanced diet or lack of physical exercise during their life course has been recognised to increase risk of this pathological condition. Recent evidence suggests that this may involve alterations in the settings of the circadian clock system, which consists of oscillating molecular pacemakers found not only in the hypothalamic region of the brain but also in most peripheral tissues, and of the hypothalamic-pituitary-adrenal (HPA) axis which regulates stress responses. These two systems are now known to interact to produce an integrated response to environmental challenges. In this review, we highlight the importance of environmental cues during early development in establishing the homeostatic set-points of the circadian clock and HPA stress systems. These effects can operate within the normal range and are not in themselves pathological, but can nevertheless affect an individual's response to environmental challenges in adult life and thus their risk of the metabolic syndrome.
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9.
Epigenetic mechanisms elicited by nutrition in early life.
Canani, RB, Costanzo, MD, Leone, L, Bedogni, G, Brambilla, P, Cianfarani, S, Nobili, V, Pietrobelli, A, Agostoni, C
Nutrition research reviews. 2011;(2):198-205
Abstract
A growing number of studies focusing on the developmental origin of health and disease hypothesis have identified links among early nutrition, epigenetic processes and diseases also in later life. Different epigenetic mechanisms are elicited by dietary factors in early critical developmental ages that are able to affect the susceptibility to several diseases in adulthood. The studies here reviewed suggest that maternal and neonatal diet may have long-lasting effects in the development of non-communicable chronic adulthood diseases, in particular the components of the so-called metabolic syndrome, such as insulin resistance, type 2 diabetes, obesity, dyslipidaemia, hypertension, and CVD. Both maternal under- and over-nutrition may regulate the expression of genes involved in lipid and carbohydrate metabolism. Early postnatal nutrition may also represent a vital determinant of adult health by making an impact on the development and function of gut microbiota. An inadequate gut microbiota composition and function in early life seems to account for the deviant programming of later immunity and overall health status. In this regard probiotics, which have the potential to restore the intestinal microbiota balance, may be effective in preventing the development of chronic immune-mediated diseases. More recently, the epigenetic mechanisms elicited by probiotics through the production of SCFA are hypothesised to be the key to understand how they mediate their numerous health-promoting effects from the gut to the peripheral tissues.
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10.
[Association between vitamin D deficiency and metabolic syndrome].
Querales, MI, Cruces, ME, Rojas, S, Sánchez, L
Revista medica de Chile. 2010;(10):1312-8
Abstract
Vitamin D has an essential role in calcium metabolism and bone health. Vitamin D3 or cholecalciferol is synthesized from 7-dehydrocholesterol or provitamin D3, by sunlight ultraviolet radiation to the skin. 7-dehydrocholesterol is subsequently hydroxylated in the liver and then in the kidney to produce 1,25-(OH)2D3, the active metabolite that binds to specific receptors (VDR) in target tissues, mainly bone and intestine. Other tissues, such as the immune and cardiovascular system, have also VDR. Vitamin D deficiency can induce rickets in children and osteomalacia and osteoporosis in adults. A possible inverse association between vitamin D levels and the prevalence of metabolic syndrome has been proposed. Vitamin D deficiency increases the risk of type 1 diabetes, insulin resistance, and hypertension, key components of this syndrome. However, other studies have not confirmed this association. Further clinical and experimental studies are needed to ascertain the role of vitamin D in metabolic syndrome.