XI. STRATEGIES FOR IMPROVING DIABETES CARE D iabetes is a chronic illness that requires continuing medical care and patient self-management education to prevent acute complications and to reduce the risk of long-term complications. Diabetes care is complex and requires that many issues, beyond glycemic control, be addressed. A large body of evidence exists that supports a range of interventions to improve diabetes outcomes. These standards of care are intended to provide clinicians, patients, researchers, payors, and other interested individuals with the components of diabetes care, treatment goals, and tools to evaluate the quality of care. While individual preferences, comorbidities, and other patient factors may require modification of goals, targets that are desirable for most patients with diabetes are provided. These standards are not intended to preclude more extensive evaluation and management of the patient by other specialists as needed. For more detailed information, refer to Bode (Ed.): Medical Management of Type 1 Diabetes (1), Burant (Ed): Medical Management of Type 2 Diabetes (2), and Klingensmith (Ed): Intensive Diabetes Management (3). The recommendations included are diagnostic and therapeutic actions that are known or believed to favorably affect health outcomes of patients with diabetes. A grading system (Table 1), developed by the American Diabetes Association (ADA) and modeled after existing methods, was utilized to clarify and codify the evidence that forms the basis for the recommendations. The level of evidence that supports each recommendation is listed after each recommendation using the letters A, B, C, or E.

Standards of Medical Care in Diabetes

AMP-activated protein kinase (AMPK) is a crucial cellular energy sensor. Once activated by falling energy status, it promotes ATP production by increasing the activity or expression of proteins involved in catabolism while conserving ATP by switching off biosynthetic pathways. AMPK also regulates metabolic energy balance at the whole-body level. For example, it mediates the effects of agents acting on the hypothalamus that promote feeding and entrains circadian rhythms of metabolism and feeding behaviour. Finally, recent studies reveal that AMPK conserves ATP levels through the regulation of processes other than metabolism, such as the cell cycle and neuronal membrane excitability.

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AMPK: a nutrient and energy sensor that maintains energy homeostasis

I read this book the same weekend that the Packers took on the Rams, and the experience of the latter event, obviously, colored my judgment. Although I abhor anything that smacks of being a handbook (like, \"How to Earn a Merit Badge in Neurosurgery\") because too many volumes in biomedical science already evince a boyscout-like approach, I must confess that parts of this volume are fast, scholarly, and significant, with certain reservations. I like parts of this well-illustrated book because Dr. Sj6strand, without so stating, develops certain subjects on technique in relation to the acquisition of judgment and sophistication. And this is important! So, given that the author (like all of us) is somewhat deficient in some areas, and biased in others, the book is still valuable if the uninitiated reader swallows it in a general fashion, realizing full well that what will be required from the reader is a modulation to fit his vision, propreception, adaptation and response, and the kind of problem he is undertaking. A major deficiency of this book is revealed by comparison of its use of physics and of chemistry to provide understanding and background for the application of high resolution electron microscopy to problems in biology. Since the volume is keyed to high resolution electron microscopy, which is a sophisticated form of structural analysis, but really morphology in a modern guise, the physical and mechanical background of The instrument and its ancillary tools are simply and well presented. The potential use of chemical or cytochemical information as it relates to biological fine structure , however, is quite deficient. I wonder when even sophisticated morphol-ogists will consider fixation a reaction and not a technique; only then will the fundamentals become self-evident and predictable and this sine qua flon will become less mystical. Staining reactions (the most inadequate chapter) ought to be something more than a technique to selectively enhance contrast of morphological elements; it ought to give the structural addresses of some of the chemical residents of cell components. Is it pertinent that auto-radiography gets singled out for more complete coverage than other significant aspects of cytochemistry by a high resolution microscopist, when it has a built-in minimal error of 1,000 A in standard practice? I don't mean to blind-side (in strict football terminology) Dr. Sj6strand's efforts for what is \"routinely used in our laboratory\"; what is done is usually well done. It's just that …

Methods in Enzymology.

The TRIPOD (Transparent Reporting of a multivariable prediction model for Individual Prognosis Or Diagnosis) Statement includes a 22-item checklist, which aims to improve the reporting of studies developing, validating, or updating a prediction model, whether for diagnostic or prognostic purposes. The TRIPOD Statement aims to improve the transparency of the reporting of a prediction model study regardless of the study methods used. This explanation and elaboration document describes the rationale; clarifies the meaning of each item; and discusses why transparent reporting is important, with a view to assessing risk of bias and clinical usefulness of the prediction model. Each checklist item of the TRIPOD Statement is explained in detail and accompanied by published examples of good reporting. The document also provides a valuable reference of issues to consider when designing, conducting, and analyzing prediction model studies. To aid the editorial process and help peer reviewers and, ultimately, readers and systematic reviewers of prediction model studies, it is recommended that authors include a completed checklist in their submission. The TRIPOD checklist can also be downloaded from www.tripod-statement.org.

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Transparent Reporting of a multivariable prediction model for Individual Prognosis or Diagnosis (TRIPOD): explanation and elaboration.

Non-thrombotic PE does not represent a distinct clinical syndrome. It may be due to a variety of embolic materials and result in a wide spectrum of clinical presentations, making the diagnosis difficult. With the exception of severe air and fat embolism, the haemodynamic consequences of non-thrombotic emboli are usually mild. Treatment is mostly supportive but may differ according to the type of embolic material and clinical severity.

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Guidelines on the Diagnosis and Management of Acute Pulmonary Embolism: The Task Force for the Diagnosis and Management of Acute Pulmonary Embolism of the European Society of Cardiology (ESC)

The scientist’s guide to cardiac metabolism

Brain uptake and utilization of fatty acids: Applications to peroxisomal biogenesis disorders (An International Workshop): Roundtable discussion of session 1: Fatty acid uptake by and transport in the brain

Rates of fatty acid oxidation increase rapidly in both rat heart and skeletal muscle in the early postnatal period. Therefore, we examined in heart and soleus muscle, (a) whether there were rapid changes in fatty acid transporter (FAT/CD36, FABPpm) mRNA and protein expression early in life (days 10 –36) and thereafter (days 84, 160, 365), and (b) whether the rates of fatty acid transport and the plasmalemmal content of FAT/CD36 and FABPpm were altered. Protein expression was altered rapidly from day 10–36 in both heart (FAT/CD36 only, +21%, P < 0.05)) and soleus muscle (FAT/CD36 + 100%, P < 0.05; FABPpm −20%, P < 0.05), with no further changes thereafter (P < 0.05). Rates of fatty acid transport (day 10 vs day 160) were increased in heart (+33%, P < 0.05) and muscle (+85%, P < 0.05), and were associated with concomitant increases in plasmalemmal FABPpm (+44%, P < 0.05) and FAT/CD36 (+16%, P < 0.05) in the heart, and only plasmalemmal FAT/CD36 in muscle (+90%, P < 0.05). Therefore, known changes in the rates of fatty acid oxidation in heart and muscle early in life appear to be accompanied by a concurrent upregulation in the rates of fatty acid transport and the expression of FAT/CD36 in heart and muscle, as well as an increase in plasmalemmal FAT/CD36 and FABPpm in the heart, and only plasmalemmal FAT/CD36 in soleus muscle. We speculate that the rapid upregulation of fatty acid transport rates in heart and muscle are needed to support the increased rates of fatty oxidation that have been previously observed in these tissues.

Tissue-specific and fatty acid transporter-specific changes in heart and soleus muscle over a 1-yr period.

Carbohydrates and long-chain fatty acids are the predominant substrates for cardiac energy production. While the mechanism and regulation of myocardial carbohydrate (glucose, lactate) uptake have been unraveled in detail in the 1990s, insight into fatty acid uptake originates from more recent studies. Fatty acid movement across the sarcolemma is facilitated by membrane-associated proteins, specifically CD36, membrane-associated fatty acid-binding protein (FABPpm) and selected fatty acid transport protein (FATP) isoforms, and is up- or downregulated through changes in sarcolemmal content of (primarily) CD36. The recruitment of CD36 from an endosomal storage pool to the sarcolemma, which is under the control of various physiological stimuli (including insulin and contraction), represents a pivotal step in the overall regulation of myocardial fatty acid uptake and utilization. Dysregulation of the intracellular cycling of CD36 underlies various cardiac metabolic diseases. As a result, the mechanism and regulation of myocardial glucose uptake by GLUT4 cycling and of fatty acid uptake by CD36 cycling are very similar. Likely, manipulation of the presence and/or activity of substrate transporters for glucose and fatty acids in the sarcolemma holds promise as therapeutic approach to alter cardiac substrate preference in disease so as to regain metabolic homeostasis and rectify cardiac functioning.

Control of Myocardial Fatty Acid Uptake

Assessment of chest pain in general practice is challenging. General practitioners (GPs) often feel uncertainty when dealing with chest pain. The role of new diagnostic tools is yet unclear. Therefore, we aimed to learn: (1) whether or not GPs experience a change in incidence and presentation of chest pain, (2) how GPs deal with uncertainty, and (3) which thoughts, demands and doubts concerning new diagnostic tools occur. Semi-structured, face to face interview based study, aiming at six main subjects: experienced changes in prevalence of chest pain, the management of chest pain patients, dealing with uncertainty, the GPs’ approach in referring chest pain patients, GPs’ attitude towards ‘unnecessary’ referrals, and the GPs’ suggestions for improving the management of chest pain patients. 145 GPs in Belgium and the Netherlands were invited to participate, 27 (15 Flemish and 12 Dutch) GPs were interviewed. Data saturation was reached. The number of patients having an acute coronary syndrome among chest pain patients is decreasing, whereas the presentation of atypical complaints increases, together leading to more uncertainty. GPs rely on their own judgment above all, and desire new diagnostic tools only when these tools are of proven added value. The incidence of chest pain in general practice is not decreasing according to the GPs. However, the presentation of chest pain is changing. GPs feel relatively comfortable with referring a considerable number of chest pain patients without ACS, as over-referral is safe. Uncertainty is regarded as a substantial element of their profession. New diagnostic tools are awaited with cautiousness.

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Jan F. C. Glatz

Papers

The scientist’s guide to cardiac metabolism

Brain uptake and utilization of fatty acids: Applications to peroxisomal biogenesis disorders (An International Workshop): Roundtable discussion of session 1: Fatty acid uptake by and transport in the brain

Tissue-specific and fatty acid transporter-specific changes in heart and soleus muscle over a 1-yr period.

Control of Myocardial Fatty Acid Uptake

Managing chest pain patients in general practice: an interview-based study.