Tuesday , August 21 2018
Home / Resources / Clinical Gems (page 2)

Clinical Gems

Our clinical gems come from the top selling medical books, and text books because knowledge is everything when it comes to diabetes.

International Textbook of Diabetes Mellitus, 4th Ed., Excerpt #128: Beta-Cell Mass and Function in Human Type 2 Diabetes Part 4

Incretin defect: Oral glucose elicits a greater insulin response than does intravenous glucose. As first demonstrated by Nauck et al., when tested at matched plasma glucose concentrations (iso- glycemic protocol) the oral route of glucose administration induces a robust increment in insulin secretion as compared with the intravenous route. In nondiabetic subjects, such potentiation — named incretin effect — averages 50 – 70% with a standard (75 g) oral glucose load, and increases with the size of the glucose load. As depicted in Figure 24.10, the incretin effect is characteristically lost in patients with T2DM.

Read More »

International Textbook of Diabetes Mellitus, 4th Ed., Excerpt #127: Beta-Cell Mass and Function in Human Type 2 Diabetes Part 3

The dominance of beta-cell functional impairment: As discussed earlier, the available evidence indicates that an average 30% loss of beta-cells is present in the islets of patients with T2DM. However, based on a series of considerations it is unlikely that this beta-cell deficit alone is the cause of most cases of diabetes. First, in vivo assessment of beta-cell function consistently shows a greater than 50% reduction in patients with overt T2DM, a difference that is amplified when using intravenous glucose.

Read More »

International Textbook of Diabetes Mellitus, 4th Ed., Excerpt #126: Beta-Cell Mass and Function in Human Type 2 Diabetes Part 2

The role of beta-cell death and regeneration: The loss of beta-cells in T2DM has been mainly attributed to increased beta-cell death due to apoptosis and other forms of cell death, possibly driven by adverse environmental conditions and probably mediated by several intracellular mechanisms. Apoptosis is a type of programmed cell death morphologically characterized by cell rounding up, bleb formation and chromatin condensation. As a matter of fact, in autoptic pancreatic samples apoptosis has been shown to be significantly increased in both obese and lean type 2 diabetic cases as compared to BMI-matched, nondiabetic controls.

Read More »

International Textbook of Diabetes Mellitus, 4th Ed., Excerpt #125: Beta-Cell Mass and Function in Human Type 2 Diabetes Part 1

Insulin-producing beta-cells are the predominant endocrine cell type in pancreatic islets, comprising 50 – 80% of islet cells. Studies with autoptic samples, organ donor specimens, and surgical cases have found that beta-cell mass in the human pancreas may vary from 0.6 to 2.1 g, with beta-cell volume and area (relative to the pancreatic tissue) ranging from 1.1 – 2.6% and 0.6 – 1.6%, respectively.

Read More »

International Textbook of Diabetes Mellitus, 4th Ed., Excerpt #124: The Insulin Resistance Syndrome Part 5

When designing any risk scoring system, those proposing such a score must weigh up various competing factors. Metabolic syndrome benefits from the inclusion of clear (and now unambiguous, with the exception of waist circumference) criteria. However equal weighting is given to the five criteria while it is known that they do not contribute equally to the development of cardiometabolic disease. As noted above, two of the five criteria are strongly linked to cardiovascular disease but only weakly to risk of developing diabetes.

Read More »

International Textbook of Diabetes Mellitus, 4th Ed., Excerpt #123: The Insulin Resistance Syndrome Part 4

The foregoing observations have detailed the best established risk factors associated with insulin resistance as well some novel emerging risk factors as additionally detailed in Table 23.2, including nutritional measures such as Vitamin D. These are not comprehensive but rather a selection of emerging pathways of interest. Clearly, future research should increasingly harness genetics as well as observational data to better determine causal risk pathways. Similarly, further data are needed to better determine the extent to which insulin resistance is, or is not, linked to cardiovascular risk.

Read More »

International Textbook of Diabetes Mellitus, 4th Ed., Excerpt #122: The Insulin Resistance Syndrome Part 3

Adipose-derived markers and insulin resistance: Whilst rising BMI or waist circumference are clearly linked to insulin resistance and risk for T2DM, a number of adipose-derived factors have attracted interest with respect to determining insulin resistance. Adiponectin, as recently reviewed, has been the most notable of these biomarkers. Adiponectin is unlike the other adipocyte hormones in that its concentrations decline with rising obesity. Therefore low levels predict higher risk for T2DM but there are a number of complexities in this relationship.

Read More »

International Textbook of Diabetes Mellitus, 4th Ed., Excerpt #121: The Insulin Resistance Syndrome Part 2

Concept of ectopic fat as a cause of tissue insulin resistance: It appears that individuals prone to T2DM (based in part on their nonmodifiable characteristics) show a greater propensity to accumulate visceral or ectopic fat for a given weight. Interestingly this characteristic, in turn, may be a downstream consequence of “impaired” subcutaneous fat storage capacity, the mechanisms of which deserve further research. As an extreme example of this concept, lipodystrophic individuals have an impaired ability to store subcutaneous fat and, as a consequence, they accumulate fat in visceral and ectopic tissues and so have marked insulin resistance.

Read More »

International Textbook of Diabetes Mellitus, 4th Ed., Excerpt #120: The Insulin Resistance Syndrome Part 1

What is insulin resistance? Broadly, insulin resistance can be defined as an abnormal biologic response to insulin; insulin, whether endogenous or exogenous in origin, has limited ability to reverse a hyperglycemic metabolic state.Thus a person with insulin resistance is, almost inevitably, progressing towards developing frank type 2 diabetes (T2DM) if an intervention (usually lifestyle) is not implemented. Due to the very close link between diabetes and insulin resistance, no formal clinical definition of insulin resistance has emerged.We will discuss the potential clinical use of the insulin resistance syndrome and the metabolic syndrome later in the chapter. For now, we focus on investigation of insulin resistance as a useful entity for research concepts, and in particular discuss its biologic consequences by describing its associated risk factor perturbations.

Read More »

International Textbook of Diabetes Mellitus, 4th Ed., Excerpt #119: Diabetes and Sleep Apnea Part 9

OSA management: OSA should be treated promptly and the aim of treatment is to reduce the morbidity and mortality associated with this condition. Weight loss and positional treatment (i.e., avoiding the position in which most episodes occur, which is usually the supine position) are important aspects of treatment. As with all obesity-related disorders, weight loss (regardless of the means) can result in significant improvements in OSA. In a randomized controlled trial of intensive lifestyle intervention in 264 patients with OSA and T2DM (the Sleep AHEAD study), weight loss of 11 kg on average in the treatment group resulted in a reduction in the AHI of about 10 events per hour.

Read More »