肠内营养的剂量（Dosing of Enteral Feeding）

1．在开始营养支持治疗时应当明确肠内营养的目标（定义为能量需求）（C级）。能量需求可以根据预测公式计算或间接测热法测定。使用预测公式应慎重，因为与间接测热法相比，预测公式对个体能量需求的判断欠准确。对于肥胖患者，如果没有间接测热法，预测公式的准确性更差（E级）     

Feeding jejunostomy: is there enough evidence to justify its routine use?

BACKGROUND AND AIM: Intraoperative placement of feeding jejunostomy is a well-established method of providing access to enteral feeding. However, some studies describe serious complications related to this procedure. A retrospective study was undertaken to look at the technical complications related to the procedure. PATIENTS AND METHODS: Patients undergoing feeding jejunostomy in the thoracic and upper gastrointestinal surgical units at the Royal Victoria Hospital between January 1998 and December 1998 were included in the study. The charts of all the patients were studied retrospectively. RESULTS: Forty-two patients underwent a feeding jejunostomy in the time period studied. Thirty-one patients had a jejunostomy as an adjunct to major oesophageal or gastric surgery. In 5 patients, feeding jejunostomy was performed in conjunction with other palliative procedures and in 6 patients, it was performed as a sole procedure. Nine (21.4%) patients had procedure-related complications. Of these, 7 (16.7%) were minor including dislodgment of the tube (n = 4), blocked tube (n = 2), and intraoperative catheter damage (n = 1). Two (4.7%) patients had major complications requiring emergency laparotomy. One of these patients died as a result of a procedure- related complication. CONCLUSION: Feeding jejunostomy is associated with high morbidity and mortality. Its routine use may not be justified in the absence of evidence to support its use.     

Induction of Cytosolic Phospholipase A2α Is Required for Adipose Neutrophil Infiltration and Hepatic Insulin Resistance Early in the Course of High-Fat Feeding

In established obesity, inflammation and macrophage recruitment likely contribute to the development of insulin resistance. In the current study, we set out to explore whether adipose tissue infiltration by neutrophils that occurs early (3 days) after initiating a high-fat diet (HFD) could contribute to the early occurrence of hepatic insulin resistance and to determine the role of cytosolic phospholipase A₂α (cPLA₂α) in this process. The 3-day HFD caused a significant upregulation of cPLA₂α in periepididymal fat and in the liver. A specific antisense oligonucleotide (AS) effectively prevented cPLA₂α induction, neutrophil infiltration into adipose tissue (likely involving MIP-2), and protected against 3-day HFD–induced impairment in hepatic insulin signaling and glucose over-production from pyruvate. To sort out the role of adipose neutrophil infiltration independent of cPLA₂α induction in the liver, mice were injected intraperitoneally with anti–intracellular adhesion molecule-1 (ICAM-1) antibodies. This effectively prevented neutrophil infiltration without affecting cPLA₂α or MIP-2, but like AS, prevented impairment in hepatic insulin signaling, the enhanced pyruvate-to-glucose flux, and the impaired insulin-mediated suppression of hepatic glucose production (assessed by clamp), which were induced by the 3-day HFD. Adipose tissue secretion of tumor necrosis factor-α (TNF-α) was increased by the 3-day HFD, but not if mice were treated with AS or ICAM-1 antibodies. Moreover, systemic TNF-α neutralization prevented 3-day HFD–induced hepatic insulin resistance, suggesting its mediatory role. We propose that an acute, cPLA₂α-dependent, neutrophil-dominated inflammatory response of adipose tissue contributes to hepatic insulin resistance and glucose overproduction in the early adaptation to high-fat feeding.Established obesity, particularly if associated with insulin resistance–related morbidities, is characterized by systemic and adipose tissue inflammation (1–3). The complexity of the adipocytokines and inflammatory cell types involved in adipose inflammation is constantly increasing, and today, most myeloid cell types have been implicated in the process, including macrophages, B cells, various T-cell classes, and even eosinophils and mast cells (4–6). In contrast, much less is known about adipose tissue and liver adaptation to a short-term high-fat diet (HFD) before overt obesity is present. Metabolically, it appears that hepatic insulin resistance may be a front-line response to a short-term (3 days) HFD (7,8), representing “physiological adaptation” and/or an early maladaptive response on the causal pathway to obesity-induced whole-body insulin resistance. It currently remains unclear to what degree this early response to an HFD involves immune cells in general and, specifically, in adipose tissue.In a previous study, we demonstrated that during the first week of initiating an HFD, adipose tissue is infiltrated by neutrophils (9). Adipose tissue protein levels of the neutrophil-specific myeloperoxidase (MPO) were increased, and correspondingly, histology detected an increased number of neutrophils within the parenchyma of adipose tissue (i.e., not restricted to blood vessels). This early appearance of neutrophils in adipose tissue was recently confirmed (10), suggesting that adipose tissue inflammation in obesity largely follows the classical inflammation paradigms of acute versus chronic inflammatory cell infiltrates, predominated first by neutrophils, then lymphocytes in the subacute period, and finally, by mononuclear macrophages when inflammation becomes chronic. Yet, the co-occurrence of increased adipose neutrophil infiltration (9,10) with the early hepatic insulin resistance (7,8) prompts the question of whether the former phenomenon is causative for the latter.Cytosolic phospholipase A₂α (cPLA₂α) has received much attention as a key regulator of inflammation. It plays a major role in the stimulus-initiated production of eicosanoids (prostaglandins and the chemoattractant leukotrienes) and platelet activating factor (11). In a previous study, we demonstrated that cPLA₂α is upregulated in vascular endothelial cells in adipose tissue of mice in response to the 3-day HFD and that it mediates the elevated expression of the endothelial intracellular adhesion molecule (ICAM-1) (12) that is used for adhesion by neutrophils and monocytes. In addition, cPLA₂α has been demonstrated to regulate superoxide generation by NADPH oxidase activation (13), thus promoting phagocyte-induced oxidative stress. Intriguingly, in humans, even a single exposure to a high-fat meal induced NADPH activation and inflammatory cascades in circulating leukocytes (14–16). These findings suggest that cPLA₂α could participate in priming/activation of circulating cells upstream in inflammatory cascades that ultimately lead to adipose tissue infiltration by neutrophils, way before obesity has developed. In the current study, we set out to reveal the role of cPLA₂α and adipose tissue neutrophil infiltration in the acute adaptation to a 3-day HFD, with emphasis on whether these early inflammatory responses could underlie the development of hepatic insulin resistance.