Maternal dietary n‐6/n‐3 fatty acid ratio affects type 1 diabetes development in the offspring of non‐obese diabetic mice

Kagohashi, Yukiko; Abiru, Norio; Kobayashi, Masakazu; Hashimoto, Michio; Shido, Osamu; Otani, Hiroki

doi:10.1111/j.1741-4520.2010.00296.x

Cited by 15 publications

(25 citation statements)

References 44 publications

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“…The offspring of mice fed on a low omega-6/omega-3 (n − 6/n − 3) EFA ratio diet showed a decrease in T1D incidence [43]. Similarly, omega-3 reduced the incidence of T1D in genetically susceptible children, indicating its benefit as a supplement to assist in the prevention of human T1D [44].…”

Section: Dietmentioning

confidence: 96%

“…Vitamin D protects from T1D in NOD mice [35,36] Reduced incidence of T1D in equatorial regions of high sunlight UV-B is essential for the synthesis of vitamin D Vitamin D supplementation: at birth protected from T1D; recent-onset T1D had no significant protection [38,39] Vitamin D has anti-inflammatory effects Omega-3 fatty acids protect from T1D in NOD mice [43] Reduced incidence of T1D in ethnic groups with a culture of increased fish consumption Omega 3 fatty acids are anti-inflammatory Omega-3 supplementation: in genetically susceptible children, T1D incidence was reduced; in pregnant mothers and their HLA higher T1D risk babies efficacy not yet known [44]; trials is on-going…”

Section: Role Of Environmentmentioning

confidence: 98%

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Advances in our understanding of the pathophysiology of Type 1 diabetes: lessons from the NOD mouse

2013

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T1D (Type 1 diabetes) is an autoimmune disease caused by the immune-mediated destruction of pancreatic β-cells. Studies in T1D patients have been limited by the availability of pancreatic samples, a protracted pre-diabetic phase and limitations in markers that reflect β-cell mass and function. The NOD (non-obese diabetic) mouse is currently the best available animal model of T1D, since it develops disease spontaneously and shares many genetic and immunopathogenic features with human T1D. Consequently, the NOD mouse has been extensively studied and has made a tremendous contribution to our understanding of human T1D. The present review summarizes the key lessons from NOD mouse studies concerning the genetic susceptibility, aetiology and immunopathogenic mechanisms that contribute to autoimmune destruction of β-cells. Finally, we summarize the potential and limitations of immunotherapeutic strategies, successful in NOD mice, now being trialled in T1D patients and individuals at risk of developing T1D.

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Section: Dietmentioning

confidence: 96%

Section: Role Of Environmentmentioning

confidence: 98%

Advances in our understanding of the pathophysiology of Type 1 diabetes: lessons from the NOD mouse

2013

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“…The milk sample was harvested from the stomach of some offspring (n56) as described previously (8) and stored at 280˚C until performance of assays. To determine the nutritional status of the offspring during infancy, some male offspring were sacrificed at weaning, and these offspring were assigned to one of two groups: dams fed the CD during lactation (C group, n56) or dams fed the HD during lactation (H group, n56).…”

Section: Animals and Dietsmentioning

confidence: 99%

High Dietary Fat Intake during Lactation Promotes Development of Diet-Induced Obesity in Male Offspring of Mice

Tsuduki

Kitano

Honma

et al. 2013

J Nutr Sci Vitaminol

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SummaryThe maternal nutritional status during pregnancy and lactation influences the risk of obesity in offspring, but the details of this phenomenon are unclear. In particular, there is little information on the influence on the offspring of the maternal nutritional status during lactation only. Therefore, in this study, we examined the influence of high dietary fat intake in dams during lactation on the risk of obesity in offspring, using C57BL/6J mice. The mice were fed a control diet (CD) during pregnancy. After birth, dams were fed a CD or a high-fat diet (HD) during lactation (3 wk). Fat and energy were significantly increased in milk from dams fed a HD during lactation. Male offspring were weaned at 3 wk old and fed a CD for 4 wk, which resulted in no significant difference in their physique. Four weeks after weaning, the offspring (7 wk old) were fed a CD or HD for 4 wk to induce obesity. High dietary fat intake in dams and offspring promoted lipid accumulation in white adipose tissue and adipocyte hypertrophy in male offspring. The underlying mechanism may involve an increase in expression of Lpl and a decrease in expression of Hsl in white adipose tissue of offspring. In conclusion, our results show that high dietary fat intake during lactation promotes development of diet-induced obesity in male offspring. Key Words lactation, high-fat diet, offspring, obesity, adipocyte hypertrophy E-mail: tsudukit@m.tohoku.ac.jp Abbreviations: Acc, acetyl-CoA carboxylase; C, offspring at weaning from dams fed CD during lactation; C-CD, dams fed CD during lactation and offspring fed CD; CD, control diet; Cd36, cluster of differentiation 36; C-HD, dams fed CD during lactation and offspring fed HD; Fas, fatty acid synthase; G6p-dh, glucose-6-phosphatate dehydrogenase; Gapdh, glyceraldehyde-3-phosphate dehydrogenase; Glut4, glucose transporter type 4; H, offspring at weaning from dams fed HD during lactation; HD, high-fat diet; H-CD, dams fed HD during lactation and offspring fed CD; H-HD, dams fed HD during lactation and offspring fed HD; Hsl, hormone sensitive lipase; Lpl, lipoprotein lipase; Me, malic enzyme; NEFA, non-esterified acid; PL, phospholipid; Pparg, peroxisome proliferator-activated receptor g; qRT-PCR, quantitative reverse transcriptase-PCR; SE, standard errors; Srebp-1c, sterol regulatory element binding protein-1c; TC, total cholesterol; TG, triacylglycerol.

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“…the influence of the maternal environment may not be straightforward). In our other articles in this issue, as an extension of a series of studies on the effect of environmental factors on the life‐long history of pathogenesis and the clinical course of genetically predisposed type 1 diabetes, we report the effect of maternal nutrition, in particular the n‐6/n‐3 fatty acid ratio, on the development of type 1 diabetes in the NOD mouse offspring (Kagohashi et al . 2010) and a preventive effect of the dietary n‐6/n‐3 fatty acid ratio even after the onset of overt diabetes (Kagohashi and Otani 2010).…”

Section: Genetic Background Versus Maternal Environment In Generationmentioning

confidence: 99%

Individual variation in organ histogenesis as a causative factor in the developmental origins of health and disease: Unnoticed congenital anomalies?

Otani

Udagawa

Hatta

et al. 2010

Congenital Anomalies

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Morphological studies of congenital anomalies have mainly focused on abnormal shape (i.e. malformation) and thus on disturbed organogenesis. However, in regard to postnatal functions of organs that develop through branching mechanisms, organ size is another important morphological feature. These organs consist of a large number of structural and functional units, such as nephrons in the kidney, and the total number of these units, that is approximately proportional to the organ size, has been shown to vary widely among individuals. Organ‐specific cells are differentiated and organized to form structural units and realize organ‐specific functions during the histogenetic period (i.e. from mid‐gestation to the early postnatal period). The total number of units is attained at the end of histogenesis and determines the total functional capacity, including the functional reserve of the organ, and thus may be related to predispositions to postnatal organ‐based diseases, because the functional reserve decreases during the course of life and eventually become short of the minimum requirement of each organ. Therefore, it may be hypothesized that a smaller number of units of organs at the end of histogenesis is one of the predisposing factors for postnatal diseases (i.e. a form of unnoticed but late‐manifested congenital anomalies), in this era of extended longevity. However, the mechanisms that control the total number of units in each organ during histogenesis and the possible relationship among the numbers of units in different organs remain unknown. Here, we review our trials based on the above hypothesis in order to (1) mathematically analyze the morphometric data of the different organs in fetuses to elucidate relationship among developing organs, (2) analyze the developing neuro‐immuno‐endocrine network as a series of mechanisms to systemically correlate the histogenesis of multiple organs, and (3) examine the maternal environment, including dietary fat, as a factor to influence histogenesis and thus the predisposition to type 1 diabetes.

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Maternal dietary n‐6/n‐3 fatty acid ratio affects type 1 diabetes development in the offspring of non‐obese diabetic mice

Cited by 15 publications

References 44 publications

Advances in our understanding of the pathophysiology of Type 1 diabetes: lessons from the NOD mouse

Advances in our understanding of the pathophysiology of Type 1 diabetes: lessons from the NOD mouse

High Dietary Fat Intake during Lactation Promotes Development of Diet-Induced Obesity in Male Offspring of Mice

Individual variation in organ histogenesis as a causative factor in the developmental origins of health and disease: Unnoticed congenital anomalies?

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