Prolonged exclusive breastfeeding reduces autoimmune diabetes incidence and increases regulatory T‐cell frequency in bio‐breeding diabetes‐prone rats

Brugman, Sylvia; Visser, J.H.M.; Hillebrands, Jan-Luuk; Bos, Nicolaas A.; Rozing, Jan

doi:10.1002/dmrr.953

Cited by 28 publications

(21 citation statements)

References 23 publications

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“…We observed a significant prevention in reduction of this enzyme activity in the 21‐day‐old pups, whose mothers were treated with Met + Mel, suggesting that the youngest pups who were nursing until this age had maternal protection. A study showed that nursing improves immunity and prevents offspring diseases: prolonged exclusive breastfeeding reduces autoimmune diabetes incidence and increases regulatory T‐cell frequency in bio‐breeding diabetes‐prone rats (Brugman et al, 2009). Our results suggested that melatonin treatment may be sufficient to prevent detectable damage through 21 days but not through 30 days.…”

Section: Discussionmentioning

confidence: 99%

The neuroprotective role of melatonin in a gestational hypermethioninemia model

Figueiró¹,

Moreira²,

Santos³

et al. 2019

Intl J of Devlp Neuroscience

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Elevated levels of methionine in blood characterize the hypermethioninemia, which may have genetic or non‐genetic origin, as for example from high protein diet. Born rats from hypermethioninemic mothers presented cerebral oxidative stress, inhibition of Na+,K+‐ATPase, memory deficit and ultrastructure cerebral changes. Melatonin is a hormone involved in circadian rhythm and has antioxidant effects. The aim of this study was to verify the possible neuroprotective effects of melatonin administration in hypermethioninemic pregnant rats on damage to biomolecules (Na+,K+‐ATPase, sulfhydryl content and DNA damage index) and behavior (open field, novel object recognition and water maze tasks), as well as its effect on cells morphology by electron microscopy in offspring. Wistar female rats received methionine (2.68 μmol/g body weight) and/or melatonin (10 mg/kg body weight) by subcutaneous injections during entire pregnancy. Control rats received saline. Biochemical analyzes were performed at 21 and 30 days of life of offspring and behavioral analyzes were performed only at 30 days of age in male pups. Results showed that gestational hypermethioninemia diminished Na+,K+‐ATPase activity and sulfhydryl content and increased DNA damage at 21 and 30 days of life. Melatonin was able to totally prevent Na+,K+‐ATPase activity alteration at 21 days and partially prevent its alteration at 30 days of rats life. Melatonin was unable in to prevent sulfhydryl and DNA damage at two ages. It also improved DNA damage, but not at level of saline animals (controls). Regarding to behavioral tests, data showed that pups exposed to gestational hypermethioninemia decreased reference memory in water maze, spent more time to the center of the open field and did not differentiate the objects in the recognition test. Melatonin was able to prevent the deficit in novel object recognition task. Electron microscopy revealed ultrastructure alterations in neurons of hypermethioninemic at both ages of offspring, whose were prevented by melatonin. These findings suggest that melatonin may be a good neuroprotective to minimize the harmful effects of gestational hypermethioninemia on offspring.

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Section: Discussionmentioning

confidence: 99%

The neuroprotective role of melatonin in a gestational hypermethioninemia model

Figueiró¹,

Moreira²,

Santos³

et al. 2019

Intl J of Devlp Neuroscience

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“…Formula feeding has been associated with various inflammatory and autoimmune diseases. 37 In contrast, breastfeeding, through its effects on the microbiome, has been associated with a protective role against asthma, autism spectrum disorder, and type 1 diabetes. 27,37 …”

Section: Environmental Factorsmentioning

confidence: 99%

Influence of Early Life, Diet, and the Environment on the Microbiome

Dong

Gupta

2019

Clinical Gastroenterology and Hepatology

157

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Advances in sequencing technology and bioinformatics have greatly enhanced our ability to understand the human microbiome. Over the last decade, a growing body of literature has linked nutrition and the environment to the microbiome and is now thought to be an important contributor to overall health. This paper reviews the literature from the past 10 years to highlight the influence of environmental factors such as diet, early life adversity and stress in shaping and modifying our microbiome towards health and disease. The review shows that many factors such as the mode of delivery, breast milk, stress, diet and medications can greatly influence the development of our gut microbiome and potentially make us more prone to certain diseases. By incorporating environmental factors into models that study the microbiome in the setting of health and disease, may provide a better understanding of disease and potentially new areas of treatment. To highlight this, we will additionally explore the role of the environment and the microbiome in the development of obesity and functional bowel disorders.

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“…Additional candidate mechanisms may involve reduced gut permeability, induction of the maturation of regulatory T cells in the gut-associated lymphoid tissue and/or modification of the gut microflora. Supporting these possibilities, it was shown that a highly hydrolyzed formula induced a decrease in autoimmune diabetes in the diseaseprone BioBreeding rat, in association with improved integrity of the intestinal barrier, production of regulatory cytokines and beneficial changes in gut microflora [32,33]. It is also possible that other elements of diet diversification such as cereal proteins may be at play, as suggested by some animal models [34,35].…”

Section: Which Are the Environmental Factors At Play?mentioning

confidence: 95%

Infectious triggers in type 1 diabetes: is there a case for epitope mimicry?

Afonso

Mallone

2013

Diabetes Obesity Metabolism

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Environmental factors are the main contributors to type 1 diabetes (T1D) pathogenesis, yet they remain unidentified. Enteroviruses are proposed candidate triggers due to temporal correlations between infection and T1D autoimmunity and to detection of viral proteins in diseased islets. However, such correlations are not universal and may be relatively uncommon. Furthermore, evidence of a cause-effect relationship is lacking, as infection of non-obese diabetic mice with Coxsackie enteroviruses can either trigger or blunt disease. The proposed mechanisms are either non-antigen-specific (i.e. β-cell destruction and release of sequestered antigens, islet inflammation) or antigen-specific (i.e. epitope mimicry, by which immune responses to enteroviruses may be diverted against homologous β-cell antigens). The case for the latter mechanisms is even less stringent, as there is little evidence of promiscuous antigen recognition at the single T-cell level. Other infectious agents may thus be implicated. Demonstration of their role will require fulfilling the Koch's postulates, namely isolation of the agent preferentially in T1D patients, including before disease onset; and T1D induction when the agent is inoculated into mice. The same is needed for cross-reactive T cells to support epitope mimicry mechanisms. Generation of alternative (humanized) mouse models that could be challenged with candidate microbes is needed. Keywords: antigen, autoimmunity, enterovirus, epitope, NOD mouse, T cells Date submitted 22 March 2013; date of final acceptance 22 May 2013 The Role of Environmental Factors in Type 1 Diabetes PathogenesisType 1 diabetes (T1D) is a multifactorial disease in which environmental triggers act on a genetic background of predisposition to engender islet autoimmunity, leading to β-cell destruction and insulin dependency. What is the relative role of genetic and environmental factors in T1D pathogenesis? Several lines of evidence converge to support the predominant role of the latter [1]. First, a dealt of susceptible alleles have been identified at different genetic loci. While three of them, namely alleles at the DQB1, INS variable number of tandem repeats (VNTR) and PTPN22 loci carry disease odds ratios >2, all the other predisposing alleles identified confer a more modest risk. Even the DQ2 and/or DQ8 haplotypes which are more strongly associated with T1D are found in a large (∼75%) proportion of T1D patients, yet also in healthy individuals. Second, the T1D concordance between monozygotic twin pairs in which one sibling is affected is rather incomplete (∼30-65%) [2,3]. Third, migrant studies document that T1D incidence adapts to that of the hosting region rather than to that of origin [4]. Fourth, comparison between regions with the same genetic background and different environmental exposures shows largely discordant T1D prevalence. One paradigmatic example is given by urbanized Finland and the nearby rural Russian Republic of Karelia, which host genetically similar human populations, yet display a ∼sixfold ...

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Prolonged exclusive breastfeeding reduces autoimmune diabetes incidence and increases regulatory T‐cell frequency in bio‐breeding diabetes‐prone rats

Cited by 28 publications

References 23 publications

The neuroprotective role of melatonin in a gestational hypermethioninemia model

The neuroprotective role of melatonin in a gestational hypermethioninemia model

Influence of Early Life, Diet, and the Environment on the Microbiome

Infectious triggers in type 1 diabetes: is there a case for epitope mimicry?

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