Starvation ketoacidosis in pregnancy

Starvation ketosis outside pregnancy is rare and infrequently causes a severe acidosis. Placental production of hormones, including glucagon and human placental lactogen, leads to the insulin resistance that is seen in pregnancy, which in turn increases susceptibility to ketosis particularly in the third trimester. Starvation ketoacidosis in pregnancy has been reported and is usually precipitated by a period of severe vomiting. Ketoacidosis is likely to have important implications for fetal survival as ketoacidosis in women with type 1 diabetes mellitus is associated with intrauterine death.     

Survival of the starving cancer patient: a food for thought for oncologists

Patients with untreated malignant bowel obstruction usually survive less than 1 month and death is accounted by 3 components: the tumour, the obstruction and the starvation. The potential benefit of total parenteral nutrition cannot be investigated, for ethical reasons, through RCT which would include a non-fed control arm. We hypothesized that if literature would consistently confirm that untreated malignant small bowel obstruction patients survive less than 1 month, there would be no need of randomised clinical trial to study the effect of total parenteral nutrition in these patients and such approach could potentially become part of the armamentarium of the oncologist.We reviewed the last 40 years of the literature on patients with malignant small bowel obstruction receiving a palliative care and distinguished 3 groups: Group I (20 studies), patients with untreated tumour, obstruction and starvation; Group II (27 studies), patients with treatment of the obstruction only, and Group III (25 studies), patients with total parenteral nutrition and some control of the obstruction.Median survivals were about 1, 1.5 and > 3 months in the 3 groups, respectively. Data suggest that total parenteral nutrition might benefit these patients being associated with a longer survival and sometimes allowing for further oncologic therapies.In conclusion, a timely intervention through parenteral nutrition should have a priority indication in a selected group of patients with malignant bowel obstruction before the occurrence of an irreversible nutritional deterioration, This would allow patients with spontaneous remission to survive longer or to be occasionally candidate for further oncologic therapies.     

csn2基因缺失对变异链球菌饥饿耐受和寡营养环境下胞外多糖合成的影响

目的探索csn2基因缺失对变异链球菌(Streptococcus mutans,Sm)饥饿耐受和寡营养环境下胞外多糖合成的影响。方法培养Sm csn2基因的缺失菌株及回补菌株,通过设置不同浓度梯度培养基创造寡营养生长环境供其生长。生长曲线检测寡营养生长环境下Sm的生长,结晶紫染色,扫描电镜、激光共聚焦显微镜检测寡营养生长环境下Sm的生物膜表型,蒽酮硫酸法检测Sm生物膜中胞外多糖的量,实时荧光定量PCR检测胞外多糖合成相关基因的表达。结果生长曲线结果显示csn2基因缺失抑制了饥饿胁迫下Sm的生长,激光扫描共聚焦显微镜检测结果显示野生型菌株、csn2基因缺陷株、回补菌株在营养充足培养条件下所得生物膜胞外多糖/细菌比值为0.44±0.07、1.05±0.13和0.57±0.08,在寡营养条件下所得生物膜胞外多糖/细菌比值为0.93±0.24、3.05±0.21和1.32±0.46,表明csn2基因缺失增强了Sm在寡营养环境下胞外多糖的合成能力;在饥饿胁迫下,胞外多糖合成相关基因gtfB、gtfC的表达水平分别显示出2.5和1.8倍的增加,gtfD的表达水平下调2/3。结论csn2基因对Sm的生理功能及毒力特性表现出多种影响,包括饥饿耐受和胞外多糖合成,这些改变可能与csn2基因缺失引发复杂的调控网络相关。     

Glucose regulates [H](+)-amphetamine binding and NaK ATPase activity in the hypothalamus: A proposed mechanism for the glucostatic control of feeding and satiety

Binding sites for [3H](+)-amphetamine in the hypothalamus may mediate the anorectic actions of amphetamine and related phenylethylamines. To investigate further the role of these sites in the central control of appetite, the binding of [3H](+)-amphetamine to the hypothalamus and brainstem was measured following food deprivation and refeeding, the onset of genetic obesity, or the administration of 2-deoxy-D-glucose. Food deprivation for 24 to 72 hours reduced the Bmax for [3H](+)-amphetamine binding in the hypothalamus and brainstem but not in other brain areas or peripheral tissues. The decrease in hypothalamic and brainstem [3H](+)-amphetamine binding observed following food deprivation was time-dependent and rapidly reversed by brief refeeding with either rat chow or a 10% glucose solution. Moreover the changes in [3H](+)-amphetamine binding were highly correlated to corresponding alterations in blood glucose concentration. Furthermore, D-glucose, but not L-glucose increases the number of hypothalamic [3H](+)-amphetamine binding sites when administered in vivo or when added to hypothalamic slices in vitro. These data suggest that the [3H](+)-amphetamine binding site in the hypothalamus and (or) brainstem may be coupled to a central "glucostat."     

蛋白质对半饥饿大鼠肠黏膜屏障的保护作用

目的:研究大鼠半饥饿状态下肠黏膜屏障的变化与补充蛋白质对其的保护作用. 方法:将48只大鼠随机分为正常对照组、50%正常饲料组、50%正常饲料+蛋白质组.2周后处死大鼠,测定小肠黏膜超氧化物歧化酶(SOD)活性、丙二醛(MDA)、DNA含量,肠系膜淋巴结(MLN)细菌移位率和血清D.木糖水平等. 结果:50%正常饲料+蛋白质组大鼠小肠黏膜DNA含量、SOD活性明显高于50%正常饲料组(P<0.05);血清D-木糖水平和MDA含量明显低于50%正常饲料组(P<0.05).结论:大鼠半饥饿状态下,增加饲料中蛋白质比例,对半饥饿大鼠肠黏膜具有一定的保护作用.     

Refractory hypoglycemia and subsequent cardiogenic shock in starvation and refeeding: Report of three cases

ObjectiveAlthough starvation is associated with high in-hospital mortality, its related cardiac complications are not sufficiently understood. The aim of this study was to determine the clinical course and pathogenesis of cardiac complications in malnourished patients.MethodsWe reviewed three cases of hypoglycemia and hypotriglyceridemia with cardiac complications in starvation.ResultsThis report concerns three patients, respectively suffering from anorexia nervosa, esophageal carcinoma, and Parkinson's disease. Their ages ranged from 18 to 70 y, body mass index was 11.5 ± 1.5 kg/m² (mean ± SD), and the main symptom was coma. The average blood glucose level was 15.7 ± 7.8 mg/dL without any history of insulin use or diabetes mellitus. In all cases, hypoglycemia was refractory and repetitive so that continuous glucose administration was required to maintain euglycemia. Serum triglyceride and non-esterified fatty acid levels were also very low (7 ± 4 mg/dL and 10 ± 9.1 μEq/L, respectively). Levels of serum potassium, phosphate, and magnesium were almost normal at admission. The main cardiac complications included Takotsubo cardiomyopathy and cardiac arrest. All patients survived as a result of intensive treatment.ConclusionsRepetitive severe hypoglycemia without known background causes should be viewed as an important sign. Once this occurs, the administration of a much higher caloric input than usual accompanied by intensive monitoring will be required to maintain appropriate glucose levels. The early identification of such patients seems to be essential to reduce the high risk for cardiac complications during starvation and refeeding.     

Endocrine changes associated with the starvation-induced premature metamorphosis in the yellow-spotted longicorn beetle, Psacothea hilaris

Under 25 degrees C and a long day photoperiod, about half of the fourth instar Psacothea hilaris larvae molt to the fifth instar on day 13 and pupate about 18 days later; the rest pupate without a further larval molt with a mean fourth instar period of 24 days. However, starvation of fourth instar larvae exceeding a threshold weight induces premature pupation, resulting in the formation of small but morphologically normal adults. To clarify the endocrine basis for this premature pupation, hemolymph juvenile hormone (JH) and ecdysteroid titers were quantified during the fed and the starved periods. Normally fed fourth instar larvae exhibited two populations with regard to JH and ecdysteroid titers, one having JH titers ranging from 1.2 to 2.1 ng/ml through to day 13, the other, similarly high titers in the early part of the instar but low titers reaching 0.1 ng/ml on day 13. One population had ecdysteroid titers with a peak of 43 ng/ml on day 10, coinciding well with the period when some larvae normally molt to the fifth instar (day 13), the other, a small peak of 14 ng/ml on day 14 and a large peak of 70 ng/ml on day 17 coinciding well with the period just before the prepupa stage. When fourth instar larvae were starved after 4 days of feeding, JH titers decreased sharply in the next 24h and never recovered, and a small but significant increase (to 21 ng/ml) in ecdysteroid titers was observed on day 6, followed by a large peak of 63 ng/ml on day 11. Altogether, these results suggest that starvation induces a rapid decline in the JH titer, and this cues the early occurrence of a small ecdysteroid peak that commits larvae to early metamorphosis.     

Effect of PstS sub-units or PknD deficiency on the survival of Mycobacterium tuberculosis

The membrane-associated phosphate-specific transporter (Pst) complex is composed of four different proteins: PstS, PstC, PstA and PstB. The PstS component detects and binds Pi with high affinity; the PstA and PstC form transmembrane pores for Pi entry, while PstB provides energy through ATP hydrolysis. In the Mycobacterium tuberculosis genome, four different gene clusters encode three PstS, and two of each of the other sub-units. We used RT-PCR to show that these clusters represent at least three distinct operons. The pstS3-containing operon was the only one induced by lack of environmental Pi. To study the physiologic role of the different PstS sub-units and that of another potential Pi receptor, PknD, we constructed and complemented their knockout (KO) mutants. In Sauton medium, the PstS1-3 KO grew faster than the Wt or the PknD KO. Following 24?h of complete starvation, the PstS3 or PknD deficient strains died if exposed to Pi poor conditions while the PstS1 and PstS2 KO survived and still grew faster than the Wt strain. These results suggest that PstS1-3 may play a role in the regulation of M. tuberculosis growth or metabolism while PstS3 and PknD contribute to the survival of the bacteria in phosphate poor conditions.     

Serum levels of S100B are decreased in chronic starvation and normalize with weight gain

S100B protein is mainly synthesized in glial cells and modulates the balance between cell proliferation and differentiation in neurons and glial cells. However, S100B is not CNS-specific since its production was detected in numerous non-cerebral tissues e.g. adipocytes. In this study we investigated the influence of chronic fasting and subsequent weight gain on serum levels of S100B in patients with anorexia nervosa. We found that nutritional status was an important factor influencing serum levels of S100B.