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本論考は, 現今秋田に広く行われている秋田型算数・数学授業の創発からあきた型算数・数学授業の確 立に至る過程を精査して, フィンランドが目指す授業との対比によって秋田型授業の基本構造を解明する ことを主たる目的とし秋田がフィンランドの取り組みを取り入れて全国学力調査で好成績を上げたとする説(本論考で浦野説と称した)の検討を行う。 秋田の算数・数学授業がシート学習の理念を一貫して継承し, 自力解決・討論型授業として今日のあきた型授業へと発展したことを解明した。低学力時代のことにも少々触れ, また数学教育現代化運動時代の秋田がこの運動を迂回することで基礎学力を高めたことを述べた。更に, 秋田の授業の基本構造を縦糸を系統性に, 各授業は進歩主義教育観の風を受けて泳ぐ鯉のぼりに見立てた。これらの成果によって浦野説 を否定した。追記として秋田の算数・数学授業の優秀性とその継続性の根拠を記した。 The purpose of the article is to scrutinize the developmental process of Akita Mode of Math Classroom (AMMC) from its emergence to the establishment, and clarify the fundamental structure of AMMC, with the examination of, so called in this article, Urano's Thesis, which intended that AMMC got some significant positive effects on the performance in the National Achievement Test by translating teaching methods from Finland. Mathematical classroom of Akita consistently succeeded to the idea of sheet-learning, and it developed into and established AMMC, which is now prevailing in Akita. Problems on the low-performance age of Akita, and the Modernization Movement in Akita are mentioned, Moreover, I describe AMMC as a carp-shaped streamer with blowing wind of subject-centered curricula and progressive educational views. Using above mentioned examination, scrutiny and clarification, I have to deny Urano's Thesis.

text, 紀要論文 / Depaetmental Bulletin Paper

text, 紀要論文 / Depaetmental Bulletin Paper

Hepatic glycogen metabolism is impaired in diabetes. We previously demonstrated that strategies to increase liver glycogen content in a high-fat-diet mouse model of obesity and insulin resistance led to a reduction in food intake and ameliorated obesity and glucose tolerance. These effects were accompanied by a decrease in insulin levels, but whether this decrease contributed to the phenotype observed in this animal was unclear. Here we sought to evaluate this aspect directly, by examining the long-term effects of increasing liver glycogen in an animal model of insulin-deficient and monogenic diabetes, namely the Akita mouse, which is characterized by reduced insulin production. We crossed Akita mice with animals overexpressing protein targeting to glycogen (PTG) in the liver to generate Akita mice with increased liver glycogen content (Akita-PTGOE). Akita-PTGOE animals showed lower glycemia, lower food intake, and decreased water consumption and urine output compared with Akita mice. Furthermore, Akita-PTGOE mice showed a restoration of the hepatic energy state and a normalization of gluconeogenesis and glycolysis back to nondiabetic levels. Moreover, hepatic lipogenesis, which is reduced in Akita mice, was reverted in Akita-PTGOE animals. These results demonstrate that strategies to increase liver glycogen content lead to the long-term reduction of the diabetic phenotype, independently of circulating insulin.

The relationship between type 1 diabetes and hearing loss is not well known, although based on many pathological studies, type 2 diabetes induced hearing loss is associated with microcirculation problems in the inner ear. The purpose of this study was to investigate the correlation between type 1 diabetes and hearing loss through hearing function and immunohistochemical analyses using type 1 diabetic Akita or wild-type (WT) mice. The Akita mice had a significant increase in hearing thresholds, blood glucose, and insulin tolerance compared to WT mice. Histological analysis showed that the loss of cells and damage to mitochondria in the spiral ganglion neurons of Akita mice were significantly increased compared to WT. Also, the stria vascularis showed decreased thickness, loss of intermediate cells, and disturbance in blood capillary shape in the Akita mice. Moreover, a reduction in type I, II, and IV fibrocytes and Na+/K+-ATPase &alpha, 1 expression in spiral ligament was also observed. Cleaved caspase-3 expression was highly expressed in spiral ganglion neurons. In conclusion, hearing loss in type 1 diabetes is caused not only by ion imbalance and blood flow disorders of cochlear endolymph, but through the degenerative nervous system via apoptosis-mediated cell death.

Lake Hachiro in Akita Prefecture is freshwater lake since 1966. Ishii et al. (2017) firstly reported four species of freshwater ostracods; Darwinula stevensoni, Bradleytriebella lineata, Cypridopsis vidua and Candona sp.1, from Lake Hachiro collected in 2015. This is the follow-up report of distribution and occurrence of freshwater ostracods from Lake Hachiro. In addition, three species of freshwater ostracods; Physocypria nipponica, Fabaeformiscandona sp. and Candona sp.2 are newly discovered, and the first one is firstly recorded from Akita Prefecture. Therefore, to date, seven species of freshwater ostracods are record of living in Lake Hachiro.

Lake Hachiro in Akita Prefecture is freshwater lake since 1966. Unofficially, the ostracods have been recognized in Lake Hachiro since 1996; however, any information has never been published up to date. The present paper reports four species of freshwater ostracods; Darwinula stevensoni, Bradleytriebella lineata, Cypridopsis vidua and Candona sp., from Lake Hachiro collected in 2015. This is the first report of distribution and occurrence of living freshwater ostracods in Akita Prefecture.

Bakalaura darbs “Japāņu tautas tradīcijas Ogas pussalā mūsdienās: Namahage” mērķis ir veikt Ogas pussalā esošo Hadači ekimae, Sugoroku un Anzendži ciemu Namahage tradīciju izpēti un prognozēt to pārmantošanas iespējas. Darbs ir izstrādāts, apzinot vēsturiskos avotus, kas pieejami Ogas pussalas Namahage tradīcijas muzejos, un veidot lauka pētījumu trīs dažādos Ogas pussalas ciemos. Darbs sastāv no sešām daļām, kurās tiek izpētītas Japānas Oga no Namahage tradīcijas vēsture, pētīto ciemu atšķirīgo un kopīgo faktoru kopsavilkums, tradīciju notiekošā situācija mūsdienās. Bakalaura darbs satur: 41 lpp. (neieskaitot titullapu, kopsavilkumu, satura rādītāju un bibliogrāfiju), 27 attēlus, 2 diagrammas un 1 tabulu., The bachelor’s theses “Japanese Folk Traditions on the Oga Peninsula Nowadays: Namahage” is a study of Namahage traditions in Hadachi ekimae, Sugroku and Anzenji communities located in Oga Peninsula to predict their inheritance possibilities. The work is based on the identification of historical sources available in the museums of Namahage in Oga Peninsula, and to conduct a field study in three different communities. The work consists of six parts, that addresses the history of the Japanese tradition Namahage, a summary what communities have individually and what they share in common, the current situation of the tradition. The bachelor's thesis contains 41 pages (without front page, summery index and bibliography), 27 figures, 2 diagrams and 1 table.

Diabetes is a major public health problem: it is estimated that 420 million people are affected globally. Monogenic forms of diabetes are less common, but variants in monogenic diabetes genes have been shown to contribute to type 2 diabetes risk. In vitro and in vivo models of monogenic forms of diabetes related to the endoplasmic reticulum (ER) stress response provided compelling evidence on the role of ER stress and dysregulated ER stress signaling on β cell demise in type 1 and type 2 diabetes. In this chapter, we describe the genetics, background, and phenotype of ER stress-related monogenic diabetes mouse models, and we comment on their advantages and disadvantages. We conclude that these mouse models are very useful tools for monogenic diabetes molecular pathogenesis studies, although there is a variability on the methodology that is used. Regarding the use of these models for therapeutic testing of ER stress modulators, a specific consideration should be given to the fact that they recapitulate some, but not all, the phenotypic characteristics of the human disease., info:eu-repo/semantics/published

We have developed a simple measuring system prototype that uses an unmanned aerial vehicle (UAV) and a non-dispersive infrared (NDIR) analyzer to detect regional carbon dioxide (CO2) concentrations and obtain vertical CO2 distributions. Here, we report CO2 measurement results for the lower troposphere above Ogata Village, Akita Prefecture, Japan (about 40&deg, N, 140&deg, E, approximately &minus, 1 m amsl), obtained with this UAV system. The actual flight observations were conducted at 500, 400, 300, 200, 100, and 10 m above the ground, at least once a month during the daytime from February 2018 to February 2019. The raw CO2 values from the NDIR were calibrated by two different CO2 standard gases and high-purity nitrogen (N2) gas (as a CO2 zero gas, 0 ppm). During the observation period, the maximum CO2 concentration was measured in February 2019 and the minimum in August 2018. In all seasons, CO2 concentrations became higher as the flight altitude was increased. The monthly pattern of observed CO2 changes is similar to that generally observed in the Northern Hemisphere as well as to surface CO2 changes simulated by an atmospheric transport model of the Japan Meteorological Agency. It is highly probable that these changes reflect the vegetation distribution around the study area.

Exploration for local varieties of wild Job's tears was undertaken on Akita prefecture and Sado island in Niigata prefectures to utilize as genetic resources of edible Job's tears. I performed exploration from October in these districts. A total of five samples of Job's tears and four samples of edible Job's tear were collected for preservation.

From Lake Hachiro in Akita Prefecture, one compound hydra, Cordylophora japonica, was reported in 1976 (Toriumi, 1976). On the other hand, Ishii has been seeing solitary hydras in Lake Hachiro since 1996, however, he had not investigated those hydras. In this report, two species of freshwater solitary hydras have been described. In this report, taxonomy of Hydras in Japan is based on the reports by Ito (1947a-d). Hydra magnipapillata and Hydra japonica collected from Lake Hachiro in 2011-2012 had been firstly reported of living in Akita Prefecture.

This paper deals with the actual conditions of physical fitness and motor ability for the youth who grew up in Akita. Physical fitness and motor ability test consist of grip strength, sit up, bending forward, side step, 20m shuttle run, 50m sprint, standing jump, and ball throw. Ministry of education, culture, sport, science and technology has conducted the survey of this test every year in the whole country. Results of the test for boys and girls in the primary, junior and senior high school were collected from the annual reports of the survey announced by the government and Akita prefecture. As for college students, we tested those who grew up in Akita in the class of physical education. These results in Akita were compared with mean values of the whole country by sex and age. Consequently, boys and girls in primary and junior high school of Akita showed a great performance as is known nationwide, except for 50m sprint. Large body size might be disadvantageous for weight movement during 50m sprint. Meanwhile, senior high school and college students in Akita demonstrated a very ordinary performance for most test items. It was thought that boys and girls in Akita would be only precocious and become ordinary people when the growth and the development are finished, although their fitness is excellent until early teens.

Elevated expression and activity of matrix metalloproteinase-9 (MMP9) and decreased contractility of cardiomyocytes are documented in diabetic hearts. However, it is unclear whether MMP is involved in the regulation of contractility of cardiomyocytes in diabetic hearts. In the present study, we tested the hypothesis that MMP9 regulates contractility of cardiomyocytes in diabetic hearts, and ablation of matrix metalloproteinase-9 (MMP9) prevents impaired contractility of cardiomyocytes in diabetic hearts. To determine the specific role of MMP9 in cardiomyocyte contractility, we used twelve - fourteen week male WT (normoglycemic sibling of Akita), Akita, and Ins2+/- /MMP9-/- (DKO) mice. DKO mice were generated by cross-breeding male Ins2+/- Akita (T1D) with female MMP9 knockout (MMP9-/-) mice. We isolated cardiomyocytes from the heart of the above three groups of mice and measured their contractility and calcium transients. Moreover, we determined mRNA and protein levels of sarco-endoplasmic reticulum calcium ATPase-2a (SERCA-2a), which is involved in calcium handling during contractility of cardiomyocytes, in WT, Akita, and DKO hearts using qPCR, Western blotting and immunoprecipitation, respectively. Our results revealed that in Akita hearts where increased expression and activity of MMP9 is reported, the rates of shortening and re-lengthening (± dL/dt) of cardiomyocytes were decreased, time to 90% peak height and baseline during contractility was increased, rate of calcium decay was increased, and calcium transient was decreased as compared to WT cardiomyocytes. However, these changes in Akita were blunted in DKO cardiomyocytes. The molecular analyses of SERCA-2a in the hearts showed that it was downregulated in Akita as compared to WT but was comparatively upregulated in DKO. These results suggest that abrogation of MMP9 gene prevents contractility of cardiomyocytes, possibly by increasing SERCA-2a and calcium transients. We conclude that MMP9 plays crucial role in the regulation of contractility of cardiomyocytes in diabetic hearts.

The Om-SK100 Tephras of early Pleistocene were possibly flowd down 450km from on-land volcanic sources in central Japan to submarine Oga region, northeast Japan. The on-land ash flows entered into water in the Niigata region, transformed into water-saturated gravity flows, namely the SK110 and SK100 Tephras in the southwestern Niigata region, 100-150km from the source. The SK110 and SK100 Tephras Beds show similar tephra sequence and consists of two divisions as the primary subflow sets. The basal division A is sand-sized and the upper division B is mostly silt-sized. The division A shows very slight decrease along down flow both in thickness and grain-size especially in the SK110 Tephra Bed throughout the Niigata region of 100-200km from the source. The gradding and lamination in the division A of the SK110 Tephra Bed are also very slight, impling the nearly plug flow condition along 0.3°-0.1° slope. In the division B of the SK110, water-escaped structures are occasionally found both in the Niigata and Akita regions of 450km from the source, impling the high-concentrated ash-cloud gravity flow origin. Thus, the division A and division B of the Om-SK110 Tephra comprise the bipartite flow deposit, and the SK100 Tephra is supposed to the similar mode of flowage. These bipartite flowage might be allowed to flow down so far as 450km from the source because of the least loss of the kinetic energy in the flow. Characterization of the parameters of these flows, comparing the case of the Joetsu Ash of typical turbulent flow deposit, was also performed.

Wild genetic resources including true indigenous populations of pear and apple species in Northern Tohoku (Aomori, Akita and Iwate prefectures) were explored and collected. A total of 33 accessions of pear and apple genetic resources, containing 17 of Pyrus ussuriensis, 10 of Malus baccata var. mandshurica, 4 of M. toringo, and 2 of M. prunifolia were collected. In Pyrus ussuriensis, indigenous type accessions were collected in highland area of the Kitakami Mountains (Iwate Pref.), where true wild populations remain. Escaped type accessions of this species were colleted in Aomori and Akita Pref., as well as in Iwate Pref. In Malus , accessions of M. baccata and M. toringo were collected from wild populations. A putative escaped population of M. prunifolia was discovered at Goshogawara, Aomori Pref.

Diabetic nephropathy (DN) is a major complication of diabetes and the leading cause of end‐stage renal disease. DN is characterized by changes in kidney structure and function but the underlying genetic and molecular factors are poorly understood. We used a mouse diversity panel to explore the genetic basis of DN traits in mice carrying the Ins2 Akita mutation. Twenty‐eight Akita strains were generated by breeding this panel to DBA/2.Akita mice. Male F1 diabetic and nondiabetic littermates were evaluated for DN‐related traits. Urine albumin‐to‐creatinine ratios (ACRs), volume and cystatin C as well as blood urea nitrogen and lipoprotein levels varied significantly among the diabetic strains. For most Akita strains, ACR values increased 2‐ to 6‐fold over euglycemic control values. However, six strains exhibited changes in ACR exceeding 10‐fold with two strains (NOD/ShiLt and CBA) showing 50‐ to 83‐ fold increases. These increases are larger than previously reported among available DN mouse models establishing these strains as useful for additional studies of renal function. ACRs correlated with cystatin C (P = 0.0286), a measure of hyperfiltration and an interstitial tubular marker associated with DN onset in humans suggesting that tubule damage as well as podocyte‐stress contributed to reduced kidney function assessed by ACR. Although large changes were seen for ACRs, severe nephropathology was absent. However, glomerular hypertrophy and collagen IV content were found to vary significantly among strains suggesting a genetic basis for early onset features of DN. Our results define the range of DN phenotypes that occur among common inbred strains of mice., Diabetic nephropathy (DN) is characterized by changes in kidney structure and function but the underlying genetic and molecular factors are poorly understood. We used a mouse diversity panel to explore the genetic basis of DN traits in mice carrying the Ins2 Akita mutation. Twenty‐eight Akita strains on different genetic backgrounds were evaluated for DN‐related traits and the results define the range of DN phenotypes that occur among common inbred strains of mice.

Le diabète est une maladie chronique dont la principale caractéristique est un niveau plasmatique élevé de glucose, qui est causé soit par un défaut dans la production d’insuline, l’action de l’insuline, ou les deux à la fois. Plusieurs études ont démontré que l’hyperglycémie chronique peut mener à la dysfonction et même la défaillance de plusieurs organes, dont le coeur, le système vasculaire, les yeux et les reins, se traduisant par des infarctus du myocarde, des accidents cérébro-vasculaires et des complications rétinales et rénales, respectivement. La néphropathie diabétique (DN) est la principale cause de déficience rénale et affecte près de 25-40% des patients diabétiques. La DN est invariablement associée à un risque élevé d’accident cérébrovasculaire et de dysfonction cardivasculaire. L’angiotensinogène (Agt) est l’unique précurseur de tous les types d’angiotensines. En plus du système rénine-angiotensine (RAS) sytémique, le rein possède son propre système intrarénal et exprime tous les composants du RAS. L’Agt est fortement exprimé dans les cellules du tubule proximal rénal (RPTC) et y est converti en angiotensine II (AngII), le peptide biologiquement actif du RAS. Les patients diabétiques présentent de hauts niveaux d’AngII et une augmentation de l’expression des gènes du RAS, suggérant que l’activation du RAS intrarénal joue un rôle important dans la progression de la DN. Les mécanismes qui contrôlent la régulation du niveau rénal d’Agt par l’hyperglycémie et l’insuline demeurent mal compris. Le but global de cette thèse est de mieux comprendre les mécanismes moléculaires qui contrôlent l’expression du gène Agt chez la souris Akita (un modèle murin de diabète de type 1). Dans cette optique, la première partie de la thèse se concentre sur deux facteurs de transcription de la famille des ribonucléoprotéines nucléaires hétérogènes (hnRNP). Chan et collaborateurs ont déjà identifié 2 protéines nucléaires hnRNP F et hnRNP K, de 48kD et 70kD respectivement. HnRNP F et hnRNP K forment un hétérodimère et se lient à l’élément de réponse à l’insuline (IRE) présent dans le promoteur du gène Agt du rat et inhibent la transcription du gène Agt in vitro. Afin de déterminer si hnRNP F / K sont responsables de l’inhibition de l’expression rénale de Agt par l’insuline in vivo, nous avons étudié des souris Akita males traités ou non avec des implants d’insuline pour une période de 4 semaines. Des souris non-Akita males ont été employées comme contrôles. Les souris Akita développent de l’hypertension et de l’hypertrophie rénale. Le traitement à l’insuline rétablit les niveaux de glucose plasmatiques et la pression systolique (SBP), et atténue l’hypertrophie rénale, l’albuminurie (ratio albumine/créatinine urinaire, ACR) et les niveaux urinaires d’Agt et AngII chez les souris Akita. De plus, le traitement à l’insuline inhibe l’expression rénale du gène Agt, tout en augmentant l’expression des gènes hnRNP F, hnRNP K et ACE2 (enzyme de conversion de l’angiotensine-2). Dans des RPTC in vitro, l’insuline inhibe Agt, mais stimule l’expression de hnRNP F et hnRNP K en présence de hautes concentrations de glucose, et ce via la voie de signalisation MAPK p44/42 (protéine kinase activée par un mitogène). La transfection avec des petits ARN interférents (siRNA) contre hnRNP F et hnRNP K prévient l’inhibition de l’expression d’Agt par l’insuline dans les RPTC. Cette étude démontre bien que l’insuline prévient l’hypertension et atténue les dommages rénaux observés chez les souris Akita diabétiques, en partie grâce à la suppression de la transcription rénale de Agt, via une augmentation de l’expression de hnRNP F et hnRNP K. La seconde partie de cette thèse change de focus et se tourne vers le facteur Nrf2 (nuclear factor erythroid 2-related factor 2). Nrf2 est un facteur de transcription qui contrôle les gènes de la réponse antioxydante cellulaire en réponse au stress oxydant ou aux électrophiles. Le but de cette étude est d’examiner l’impact de la surexpression de la catalase (Cat) dans les RPTC sur l’expression du gène Agt via Nrf2 et sur le développement de l’hypertension et des dommages rénaux résultants chez les souris diabétiques Akita transgéniques (Tg). Nos études ont démontré que la surexpression de Cat dans les souris Akita Cat-Tg normalise la SBP, atténue les dommages rénaux et inhibe l’expression des gènes Nrf2 et Agt dans les RPTC. In vitro, le glucose élevé (HG) et l’oltipraz (un activateur de Nrf2) stimulent l’expression de Nrf2 et Agt, et cet effet peut être bloqué par la trigonelline (inhibiteur de Nrf2), des siRNA contre Nrf2, des antioxydants ou des inhibiteurs pharmacologiques NF-κB et MAPK p38. La suppression de sites de réponse à Nrf2 présents dans le promoteur du gène Agt du rat abolit la stimulation par l’oltipraz. Finalement, des souris males adultes non-transgéniques traitées avec l’oltipraz montrent une augmentation de l’expression de Nrf2 et Agt dans leurs RPTC et cette augmentation peut être normalisée par la trigonelline. Ces données permettent d’identifier un nouveau mécanisme d’action de Nrf2, par la stimulation du gène Agt intrarénal et l’activation du RAS, qui induisent l’hypertension et les dommages rénaux par le glucose élevé et les espèces réactives de l’oxygène chez les souris diabétiques. Nos conclusions permettent de démontrer que l’insuline induit l’expression de hnRNP F et hnRNP K, qui jouent ensuite un rôle protecteur en prévenant l’hypertension. La surexpression de la catalase dans les RPTC vient quant à elle atténuer l’activation de Nrf2 et ainsi réduit la SBP chez les souris Akita., Diabetes mellitus is a chronic metabolic disorder characterized by high plasma glucose caused by an impairment of insulin production, insulin action or both. Accumulating evidence has shown that chronic hyperglycemia can lead to dysfunction and failure of multiple organs including the heart, vascular system, eyes, and kidneys resulting in myocardial infarction, stroke, and retinal and renal complications, respectively. Diabetic nephropathy (DN) is the leading cause of end-stage renal disease affecting approximately 25–40% of diabetic patients. DN is invariably associated with an increased risk of stroke and cardiovascular dysfunction. Angiotensinogen (Agt) is the sole precursor for all types of angiotensins. In addition to systemic renin-angiotensin system (RAS), all the components of the intrarenal RAS are expressed in the kidney. Agt is highly expressed in the renal proximal tubular cells (RPTCs) and converted into biologically active angiotensin II (Ang II). In Diabetics, intrarenal Ang II level and RAS gene expression are upregulated, suggesting that intrarenal RAS activation plays an important role in the progression of DN. The mechanism (s) underlying the regulation of renal Agt by hyperglycemia and insulin are not completely understood. The overall aim of this thesis is to understand the molecular mechanism(s) that regulate renal Agt gene expression in an Akita mouse (a mouse model of type 1 diabetes). For this purpose, the first part of this thesis focuses on two transcription factors from the heterogenous nuclear ribonucleoprotein (hnRNPs) family. Previously, Chan’s group identified two nuclear proteins hnRNP F and hnRNP K of 48kD and 70kD, respectively. hnRNP F and hnRNP K form a heterodimer and bind to the insulin-responsive element (IRE) in the rat Agt gene promoter inhibiting Agt gene transcription in vitro. To determine whether hnRNP F / K mediate insulin inhibition of renal Agt expression in vivo, we used adult male Akita mice treated ± insulin implants for 4 weeks. Non-Akita mice served as controls. The Akita mice developed hypertension and exhibited renal hypertrophy. Insulin treatment normalized plasma glucose levels and systolic blood pressure (SBP), attenuated renal hypertrophy, decreased urinary albumin/creatinine ratio (ACR) and urinary Agt and Ang II levels in Akita mice. Furthermore, insulin treatment inhibited renal Agt expression but enhanced hnRNP F, hnRNP K and angiotensinconverting enzyme-2 (ACE2) expression. In vitro, insulin inhibited Agt but stimulated hnRNP F and hnRNP K expression in high-glucose media via p44/42 mitogen-activated protein kinase signaling in RPTCs. Transfection with hnRNP F and hnRNP K small interfering RNAs (siRNA) prevented the insulin inhibition of Agt expression in RPTCs. This study demonstrates that insulin prevents hypertension and attenuates kidney injury, at least in part, through suppressing renal Agt transcription via upregulation of hnRNP F and hnRNP K expression in diabetic Akita mice. In the second part of the thesis we focused on the nuclear factor erythroid 2-related factor 2 (Nrf2). Nrf2 is a transcription factor that regulates cellular antioxidant gene defense against oxidative stress or electrophiles. The purpose of this study is to investigate the impact of the overexpressing catalase (Cat) in RPTCs on Agt gene expression via Nrf2and the resulting effects on the development of hypertension and renal injury in diabetic Akita transgenic (Tg) mice. Our studies demonstrate that Cat overexpression normalizes SBP, attenuates renal injury, and inhibits RPTC Nrf2 and Agt gene expression in the Akita Cat- Tg compared to Akita mice. In vitro, high glucose (HG) and Oltipraz stimulated Nrf2 and Agt gene expression; these changes were blocked by Trigonelline (an inhibitor of Nrf2), siRNA against Nrf2, antioxidants, or pharmacological inhibitors of NF-kB and p38 mitogen-activated protein kinase. Moreover, deletion of Nrf2-responsive elements in the rat Agt gene promoter abolishes the stimulatory effect of Oltipraz. Finally,non transgenic adult male mice treated with the Nrf2 activator Oltipraz, upregulated Nrf2 and Agt expression in mouse RPTs, an effect that was normalized by Trigonelline. These data identify a novel mechanism via which Nrf2 mediates the stimulation of intrarenal Agt gene expression and activates the RAS through whichHG/reactive oxygen species (ROS) induce hypertension and renal injury in diabetic mice. Our findings demonstrate that the insulin induced hnRNP F and hnRNP K gene expression play a protective role in the preventing hypertension. Catalase overexpression, in RPT's, attenuates Nrf2 activation and lowers the SBP in Akita mice.