核糖糖基化引起仓鼠卵巢细胞GRP75变化

<正>Dear Editor,Recently,type 2 diabetic patients were clinically observed to suffer from dysfunction not only in glucose metabolism,but also ribose[1-2].Ribose is rapidly reacted with protein[3-4],producing cytotoxic ribosylated products[5],whose progress is much faster than glucose[6-7].A 75 ku glucose regulated protein(GRP75)is generally recognized as a member of the heat shock protein 70(HSP70)class of proteins,which is induced under conditions of low glucose and other nutritional and environmental stresses[8-9].Administration of ribose induces a decrease in blood     

冷冻电子断层扫描研究原代培养神经元中的线粒体膜动态变化（英文）

<正>Dear Editor,Mitochondria acts as a cellular organelle that produces ATP and buffers Ca²⁺, and plays an important role in neuronal growth, survival and function^[1]. Loss of mitochondria will make the ATP supply insufficient, resulting in synaptic transmission dysfunction^[2]. Further, presynaptic mitochondrial dysfunctions are often associated with severe neurological diseases^[3].     

Decreased serum brain-derived neurotrophic factor in Chinese patients with Type 2 diabetes mellitus

Brain-derived neurotrophic factor （BDNF） is a member of neurotrophin family associated with the proliferation, differentiation, activity-dependent plasticity, and survival of neurons in the central nervous system [1]. BDNF influences glucose metabolism and insulin sensitivity. For example, BDNF decreases serum glucose, insulin, and HbAlc levels in diabetic rats, suggesting that the BDNF may improve insulin sensitivity. In addition, animal models showed that BDNF levels in the central nervous system are highly related to peripheral serum BDNF levels [2]. It was found that BDNF may ameliorate glucose metabolism and prevent pan- creatic exhaustion in obese diabetic mice [3].     

Letter to Editor: 雌性GK糖尿病大鼠的核糖，AGEs和转酮酶变化

<正>Dear Editor,Type 2 diabetes is a chronic disease characterized by high glucose levels in the blood. Recently, it has been found that type 2 diabetic patients suffer from glucose and ribose dysmetabolism[1-3]. The GotoKakizaki (GK) rat is a nonobese, nonhypertensive model of type 2 diabetes, which, like humans, shares a susceptibility locus on chromosome 10[4-5].     

MicroRNAs expression profiles in adipose tissues and liver from sex-linked dwarf and normal chickens

Recently, increasing evidence suggested that miRNAs contribute to the regulation of adipose deposition and fat metabolism [1-7]. Meanwhile, several studies have consistently indicated that miRNAs are involved in metabolic functions of the liver, including glucose and lipid metabolism [8-12].     

Aldosterone may induce visfatin expression via the GR-ERK1/2 signal pathway in 3T3-L1 adipocytes

The main function of aldosterone is to regulate blood pressure and electrolytic balance;however,recent studies have also focused on the effect of aldosterone on glucose metabolism especially in adipose tissue.Aldosterone was found to inhibit insulin-induced glucose uptake in 3T3-L1 adipocytes [1] and aldosterone deficiency was found to prevent high-fat-feeding-induced hyperglycemia and adipocyte dysfunction in mice [2].Visfatin,an adipokine discovered by the team of Fukuhara,is mainly released by adipose tissue [3].Treatment of 3T3-L1 adipocytes and L6 myocytes with visfatin increased basal glucose uptake,and glucose release was suppressed in H4IIEC3 hepatocytes after visfatin treatment [3].It has also been suggested that visfatin may act as a proinflammatory cytokine [4] and produce chronic inflammation in adipocytes [5].Eyileten et al.[6] reported that treatment with angiotensin-converting enzyme inhibitor,which can reduce plasma aldosterone concentration,decreased circulating visfatin level in diabetic nephropathy patients.These findings suggest a possible interaction between the renin–angiotensin–aldosterone system(RAAS)and visfatin.Considering the important roles of aldosterone and visfatin and the association between RAAS and visfatin,we hypothesize that there may be a direct regulatory interaction between aldosterone and visfatin.To test this hypothesis,3T3-L1 adipocytes were used as the cell model and the expression of visfatin was measured by qRT-PCR and western blot analysis.     

椪柑营养诊断的DRIS初步标准

自1973年Beaufils提出综合诊断施肥法(Diagnosis and Recommendation Integrated System,简称DRIS)^[1]后,Sumner等人相继制订了大豆^[2]、玉米^[3]、甘蔗^[4]、马铃薯^[5]和小麦^[6]等农作物的DRIS标准,并在生产中获得了广泛的应用。但在柑桔生产中,直到1984年Beverly等人才建立伏令夏橙的DRIS标准^[7]。而对椪柑的DRIS标准则至今尚未见报道。本文根据庄伊美等报道的福建省24个高产(亩产2000-5000公斤)椪柑园的资料^[8],试图制订椪柑的DRIS初步标准,以供生产上应用之参考。     

铅和镉污染对大羽藓生理特性的影响

This paper dealt with the effects of ²⁺,²⁺ and their combined pollution on the contents of chlorophyll,potassium and calcium in Thuidium cymbifolium.The results showed that except at 0.1 mg ²⁺稬^-1,the chlorophyll content decreased with increasing ²⁺ and ²⁺ concentrations,which was 18% of the control at 100 mg ²⁺稬^-1,and decreased by 48.6% at 200 mg ²⁺稬^-1.The potassium and calcium contents also decreased with increasing pollutants concentrations,being decreased by 61.1% at 100 mg ²⁺稬^-1.²⁺ had a stronger toxicity than ²⁺,and the toxicity of their combined pollution was stronger than that of each pollutant.²⁺ could increase the toxicity of ²⁺.     

Role for dopamine in malonate-induced damage in vivo in striatum and in vitro in mesencephalic cultures

Defects in mitochondrial energy metabolism have been implicated in the pathology of several neurodegenerative disorders. In addition, the reactive metabolites generated from the metabolism and oxidation of the neurotransmitter dopamine (DA) are thought to contribute to the damage to neurons of the basal ganglia. We have previously demonstrated that infusions of the metabolic inhibitor malonate into the striata of mice or rats produce degeneration of DA nerve terminals. In the present studies, we demonstrate that an intrastriatal infusion of malonate induces a substantial increase in DA efflux in awake, behaving mice as measured by in vivo microdialysis. Furthermore, pretreatment of mice with tetrabenazine (TBZ) or the TBZ analogue Ro 4-1284 (Ro-4), compounds that reversibly inhibit the vesicular storage of DA, attenuates the malonate-induced DA efflux as well as the damage to DA nerve terminals. Consistent with these findings, the damage to both DA and GABA neurons in mesencephalic cultures by malonate exposure was attenuated by pretreatment with TBZ or Ro-4. Treatment with these compounds did not affect the formation of free radicals or the inhibition of oxidative phosphorylation resulting from malonate exposure alone. Our data suggest that DA plays an important role in the neurotoxicity produced by malonate. These findings provide direct evidence that inhibition of succinate dehydrogenase causes an increase in extracellular DA levels and indicate that bioenergetic defects may contribute to the pathogenesis of chronic neurodegenerative diseases through a mechanism involving DA.     

Scurvy in capybaras bred in captivity in Argentine

In order to determine if the absence of vitamin C in the diet of capybaras (Hydrochoerus hydrochaeris) causes scurvy, a group of seven young individuals were fed food pellets without ascorbic acid, while another group of eight individuals received the same food with 1 g of ascorbic acid per animal per day. Animals in the first group developed signs of scurvy-like gingivitis, breaking of the incisors and death of one animal. Clinical signs appeared between 25 and 104 days from the beginning of the trial in all individuals. Growth rates of individuals deprived of vitamin C was considerably less than those observed in the control group. Deficiency of ascorbic acid had a severe effect on reproduction of another population of captive capybaras. We found that the decrease in ascorbic acid content in the diet affected pregnancy, especially during the first stages. The results obtained suggest that it is necessary to supply a suitable quantity of vitamin C in the diet of this species in captivity.     

Changes in lactate dehydrogenase activity in chicken tissues in hyperthyreosis in ontogenesis

The lactate dehydrogenase activity in reactions of lactate oxidation and synthesis was studied in subfractions of the chicken brain, heart and liver at the embryonal, early postembryonal and adult stages of development after thyroxine administration. It has been shown that during embryogenesis thyroxine predominantly enhanced the rate of lactate oxidation in the mitochondrial tissues. A marked increase in the lactate synthesis was found in cytoplasm of the adult chicken tissues. Specificity of enzyme activity alterations was detected in the chicken brain during ontogenesis after thyroxine administration.     

SSTR5 ablation in islet results in alterations in glucose homeostasis in mice

Somatostatin (SST) peptide is a potent inhibitor of insulin secretion and its effect is mediated via somatostatin receptor 5 (SSTR5) in the endocrine pancreas. To investigate the consequences of gene ablation of SSTR5 in the mouse pancreas, we have generated a mouse model in which the SSTR5 gene was specifically knocked down in the pancreatic beta cells (betaSSTR5Kd) using the Cre-lox system. Immunohistochemistry analysis showed that SSTR5 gene expression was absent in beta cells at three months of age. At the time of gene ablation, betaSSTR5Kd mice demonstrated glucose intolerance with lack of insulin response and significantly reduced serum insulin levels. Insulin tolerance test demonstrated a significant increase of insulin clearance in vivo at the same age. In vitro studies demonstrated an absence of response to SST-28 stimulation in the betaSSTR5Kd mouse islet, which was associated with a significantly reduced SST expression level in betaSSTR5Kd mice pancreata. In addition, betaSSTR5Kd mice had significantly reduced serum glucose levels and increased serum insulin levels at 12 months of age. Glucose tolerance test at an older age also indicated a persistently higher insulin level in betaSSTR5Kd mice. Further studies of betaSSTR5Kd mice had revealed elevated serum C-peptide levels at both 3 and 12 months of age, suggesting that these mice are capable of producing and releasing insulin to the periphery. These results support the hypothesis that SSTR5 plays a pivotal role in the regulation of insulin secretion in the mouse pancreas.