Effects of green tea polyphenols on inflammation and iron status.

Inflammation is an underlying problem for many disease states and has been implicated in iron deficiency (ID). This study aimed to determine whether iron status is improved by epigallocatechin-3-gallate (EGCG) through reducing inflammation. Thirty-two male Sprague-Dawley rats were fed an iron-deficient diet for 2 weeks and then randomly divided into four groups ( 8 each): positive controls, negative controls, lipopolysaccharide (LPS, 0⋅5 mg/kg body weight), and LPS + EGCG (LPS plus 600 mg EGCG/kg diet) for 3 additional weeks.

Letrozole-Induced Polycystic Ovary Syndrome Attenuates Cystathionine-β Synthase mRNA and Protein Abundance in the Ovaries of Female Sprague Dawley Rats.

Background: Polycystic ovary syndrome (PCOS) is an endocrine disorder that affects 10% of reproductive-aged women and leads to hyperandrogenism, anovulation, and infertility. PCOS has been associated with elevated serum homocysteine as well as altered methylation status; however, characterization of one-carbon metabolism (OCM) in PCOS remains incomplete.

Objectives: The aim of our research was to assess OCM in a letrozole-induced Sprague Dawley rat model of PCOS.

Maternal high-fat diet disrupted one-carbon metabolism in offspring, contributing to nonalcoholic fatty liver disease.

Background & Aims: Pregnant women may transmit their metabolic phenotypes to their offspring, enhancing the risk for nonalcoholic fatty liver disease (NAFLD); however, the molecular mechanisms remain unclear.

Methods: Prior to pregnancy female mice were fed either a maternal normal-fat diet (NF-group, "no effectors"), or a maternal high-fat diet (HF-group, "persistent effectors"), or were transitioned from a HF to a NF diet before pregnancy (H9N-group, "effectors removal"), followed by pregnancy and lactation, and then offspring were fed high-fat diets after weaning. Offspring livers were analysed by functional studies, as well as next-generation sequencing for gene expression profiles and DNA methylation changes.

Dietary Whole Egg Reduces Body Weight Gain in a Dose-Dependent Manner in Zucker Diabetic Fatty Rats.

Background: We previously reported that a whole-egg-based diet attenuated weight gain in rats with type 2 diabetes (T2D) and more effectively maintained vitamin D status than an equivalent amount of supplemental cholecalciferol.

Objectives: The objective of this study was to determine the lowest dose of whole egg effective at maintaining vitamin D homeostasis and attenuating the obese phenotype in T2D rats.

Methods: Zucker diabetic fatty (ZDF) rats (n = 40; age 6 wk; prediabetic) and their lean controls (n = 40; age 6 wk) were randomly assigned to a diet containing 20% casein (CAS) or 20%, 10%, 5%, or 2.

Dietary Egg Protein Prevents Hyperhomocysteinemia via Upregulation of Hepatic Betaine-Homocysteine S-Methyltransferase Activity in Folate-Restricted Rats.

Background: Hyperhomocysteinemia is associated with increased cardiovascular disease risk. Whole eggs contain several nutrients known to affect homocysteine regulation, including sulfur amino acids, choline, and B vitamins.

Objective: The aim of this study was to determine the effect of whole eggs and egg components (i.

Whole Egg Consumption Impairs Insulin Sensitivity in a Rat Model of Obesity and Type 2 Diabetes.

Background: The literature regarding the relation between egg consumption and type 2 diabetes (T2D) is inconsistent and there is limited evidence pertaining to the impact of egg consumption on measures of insulin sensitivity.

Objectives: The aim of this study was to investigate the effect of dietary whole egg on metabolic biomarkers of insulin resistance in T2D rats.

Methods: Male Zucker diabetic fatty (ZDF) rats ( = 12; 6 wk of age) and age-matched lean controls ( = 12) were randomly assigned to be fed a casein- or whole egg-based diet.

Whole Egg Consumption Exerts a Nephroprotective Effect in an Acute Rodent Model of Type 1 Diabetes.

Nephropathy is a well-characterized complication of type 1 diabetes (T1D), resulting in proteinuria and urinary loss of micronutrients. We previously found that a whole egg-based diet maintained vitamin D balance in type 2 diabetic rats despite excessive urinary losses due to nephropathy. The goal of this study was to investigate the impact of whole egg consumption in T1D rats.

Dietary Whole Egg Consumption Attenuates Body Weight Gain and Is More Effective than Supplemental Cholecalciferol in Maintaining Vitamin D Balance in Type 2 Diabetic Rats.

Type 2 diabetes (T2D) is characterized by vitamin D insufficiency owing to excessive urinary loss of 25-hydroxycholecalciferol [25(OH)D]. We previously reported that a diet containing dried whole egg, a rich source of vitamin D, was effective at maintaining circulating 25(OH)D concentrations in rats with T2D. Furthermore, whole egg consumption reduced body weight gain in rats with T2D.

Consumption of Dietary Resistant Starch Partially Corrected the Growth Pattern Despite Hyperglycemia and Compromised Kidney Function in Streptozotocin-Induced Diabetic Rats.

We previously demonstrated that feeding of dietary resistant starch (RS) prior to the induction of diabetes delayed the progression of diabetic nephropathy and maintained vitamin D balance in streptozotocin (STZ)-induced type 1 diabetic (T1D) rats. Here, we examined the impact of RS on kidney function and vitamin D homeostasis following STZ injection. Male Sprague-Dawley rats were administered STZ and fed a standard diet containing cornstarch or 20, 10, or 5% RS for 4 weeks.

Circulating adiponectin concentrations are increased by dietary resistant starch and correlate with serum 25-hydroxycholecalciferol concentrations and kidney function in Zucker diabetic fatty rats.

We previously reported that dietary resistant starch (RS) type 2 prevented proteinuria and promoted vitamin D balance in type 2 diabetic (T2D) rats. Here, our primary objective was to identify potential mechanisms that could explain our earlier observations. We hypothesized that RS could promote adiponectin secretion and regulate the renin-angiotensin system activity in the kidney.

Whole Egg Consumption Prevents Diminished Serum 25-Hydroxycholecalciferol Concentrations in Type 2 Diabetic Rats.

Type 2 diabetes (T2D) is characterized by vitamin D deficiency owing to increased urinary loss of 25-hydroxycholecalciferol (25D). Whole eggs are a rich source of vitamin D, particularly 25D, the circulating form that reflects status. Zucker diabetic (type 2) fatty (ZDF) rats and their lean counterparts were fed casein- or whole egg-based diets for 8 weeks.

Dietary resistant starch prevents urinary excretion of vitamin D metabolites and maintains circulating 25-hydroxycholecalciferol concentrations in Zucker diabetic fatty rats.

Background: Type 2 diabetes (T2D) is the leading cause of nephropathy in the United States. Renal complications of T2D include proteinuria and suboptimal serum 25-hydroxycholecalciferol (25D) concentrations. 25D is the major circulating form of vitamin D and renal reabsorption of the 25D-vitamin D-binding protein (DBP) complex via megalin-mediated endocytosis is believed to determine whether 25D can be activated to 1,25-dihydroxycholecalciferol (1,25D) or returned to circulation.

Epigenetics in adipose tissue, obesity, weight loss, and diabetes.

Given the role that diet and other environmental factors play in the development of obesity and type 2 diabetes, the implication of different epigenetic processes is being investigated. Although it is well known that external factors can cause cell type-dependent epigenetic changes, including DNA methylation, histone tail modifications, and chromatin remodeling, the regulation of these processes, the magnitude of the changes and the cell types in which they occur, the individuals more predisposed, and the more crucial stages of life remain to be elucidated. There is evidence that obese and diabetic people have a pattern of epigenetic marks different from nonobese and nondiabetic individuals.

Nutritional epigenomics: a portal to disease prevention.

Epigenetics can be defined as inheritable and reversible phenomena that affect gene expression without altering the underlying base pair sequence. Epigenomics is the study of genome-wide epigenetic modifications. Because gene expression changes are critical in both normal development and disease progression, epigenetics is widely applicable to many aspects of biological research.

Exercise prevents hyperhomocysteinemia in a dietary folate-restricted mouse model.

Hyperhomocysteinemia is a condition that results from altered methyl group metabolism and is associated with numerous pathological conditions. A number of nutritional and hormonal factors have been shown to influence circulating homocysteine concentrations; however, the impact of exercise on homocysteine and methyl group balance is not well understood. Our hypothesis was that exercise represents an effective means to prevent hyperhomocysteinemia in a folate-independent manner.

Dietary resistant starch prevents urinary excretion of 25-hydroxycholecalciferol and vitamin D-binding protein in type 1 diabetic rats.

Diabetes is a rapidly growing epidemic affecting millions of Americans and has been implicated in a number of devastating secondary complications. We previously demonstrated that type 2 diabetic rats exhibit vitamin D deficiency due to aberrant megalin-mediated endocytosis and excessive urinary excretion of 25-hydroxycholecalciferol (25D3) and vitamin D-binding protein (DBP). Here, we examined whether a model of type 1 diabetes [T1D; streptozotocin (STZ)-treated Sprague-Dawley rats] would similarly excrete abnormally high concentrations of 25D3 and DBP due to renal damage and compromised expression of megalin and its endocytic partner, disabled-2 (Dab2).

Homocysteine imbalance: a pathological metabolic marker.

Perturbations in methyl group metabolism and homocysteine balance have emerged over the past few decades as having defining roles in a number of pathological conditions. Numerous nutritional, hormonal, and genetic factors that are characterized by elevations in circulating homocysteine concentrations are also associated with specific pathological conditions, including cancer development, autoimmune diseases, vascular dysfunction, and neurodegenerative disease. Although much remains to be explored, our understanding of the relationship between disease, methyl balance, and epigenetic control of gene expression has steadily progressed.

Tissue-specific alterations of methyl group metabolism with DNA hypermethylation in the Zucker (type 2) diabetic fatty rat.

Background: Altered methyl group and homocysteine metabolism were tissue-specific, persistent, and preceded hepatic DNA hypomethylation in type 1 diabetic rats. Similar metabolic perturbations have been shown in the Zucker (type 2) diabetic fatty (ZDF) rat in the pre-diabetic and early diabetic stages, but tissue specificity and potential impact on epigenetic marks are unknown, particularly during pathogenesis.

Methods: ZDF (fa/fa) and lean (+/?) control rats were killed at 12 and 21 weeks of age, representing early and advanced diabetic conditions.

Insulin administration abrogates perturbation of methyl group and homocysteine metabolism in streptozotocin-treated type 1 diabetic rats.

Modifications in methyl group and homocysteine metabolism are associated with a number of pathologies, including vascular disease, cancer, and neural tube defects. A diabetic state is known to alter both methyl group and homocysteine metabolism, and glycine N-methyltransferase (GNMT) is a major regulatory protein that controls the supply and utilization of methyl groups. We have shown previously that diabetes induces GNMT expression and reduces plasma homocysteine pools by stimulating both its catabolism and folate-independent remethylation.

Dietary intake of S-(alpha-carboxybutyl)-DL-homocysteine induces hyperhomocysteinemia in rats.

Betaine homocysteine S-methyltransferase (BHMT) catalyzes the transfer of a methyl group from betaine to homocysteine (Hcy), forming dimethylglycine and methionine. We previously showed that inhibiting BHMT in mice by intraperitoneal injection of S-(alpha-carboxybutyl)-DL-homocysteine (CBHcy) results in hyperhomocysteinemia. In the present study, CBHcy was fed to rats to determine whether it could be absorbed and cause hyperhomocysteinemia as observed in the intraperitoneal administration of the compound in mice.

Homocysteine metabolism and its relation to health and disease.

Homocysteine is a metabolic intermediate in methyl group metabolism that is dependent on a number of nutritional B-vitamin cofactors. An emerging aspect of homocysteine metabolism is its relation to health and disease. Perturbations of homocysteine metabolism, particularly intracellular and subsequently circulating accumulation of homocysteine (i.

Type I diabetes leads to tissue-specific DNA hypomethylation in male rats.

Numerous perturbations of methyl group and homocysteine metabolism have been documented as an outcome of diabetes. It has also been observed that there is a transition from hypo- to hyperhomocysteinemia in diabetes, often concurrent with the development of nephropathy. The objective of this study was to characterize the temporal changes in methyl group and homocysteine metabolism in the liver and kidney and to determine the impact these alterations have on DNA methylation in type 1 diabetic rats.