Special Issue: Advancements in Diabetes


Advancements in Diabetes


Maria Luz Fernandez1, Ana Gabriela Murillo2

1Department of Nutritional Sciences, University of Connecticut, Storrs, CT, USA
2Department of Biochemistry, University of Costa Rica, San José, Costa Rica


Type 2 diabetes (T2D) has increased dramatically in the last 20 years afflicting more than 425 million people all over the world with 34 million located in the US, emphasizing the need for strategic therapies including dietary prescriptions or other lifestyle changes to reduce these numbers. In addition to abnormally high plasma glucose levels, high concentrations of glycosylated hemoglobin and insulin resistance, T2D is also characterized by dyslipidemias, oxidative stress, and low-grade systemic inflammation. Insulin resistance and inflammation in T2D can lead to cardiac problems, non-alcoholic fatty liver disease and kidney failure. T2D can be controlled by modifying current unhealthy practices by focusing on wholesome diets, exercise regimes and maintenance of a healthy body weight. In this review, we aim to demonstrate how specific dietary prescriptions including carbohydrate restriction, the Mediterranean diet, plant-based diets and the dietary approaches to treat hypertension (DASH) can improve not just the inflammatory response and reduce the biomarkers of inflammation but also have additional benefits on insulin resistance, weight loss, plasma lipids and blood pressure. In addition, the mechanistic evaluation of specific nutrients including antioxidants (polyphenols and carotenoids), certain fatty acids and vitamins and their exclusive role in decreasing inflammation will be discussed.

John Malone


Diabetes Mellitus, prolonged hyperglycemia, causes peripheral and central nervous system dysfunction.  Chronic hyperglycemia causes changes in the sorbitol, inositol and taurine content of peripheral and central nervous system tissue.  The proteins in these tissues are also altered by glycosylation end products. The changes in metabolites impair growth and development of nerves and the increased glycosylation end products make the proteins stiff, sticky and prone to physical injury.  This activity stimulated by hyperglycemia impairs the normal function of the peripheral and central nervous system.  Manifestations of this tissue injury have been loss of sensation and increased pain in the extremities, loss of proprioception when standing, dysregulation of gastrointestinal motility, and heart rate.  Also noted in children are delayed maturation of cognitive function during childhood and more rapid decline of cognitive function with increasing age and increasing HbA1c. 

Sleep apnea has become an important cause of heart failure and death commonly linked to type 2 diabetes and obesity.  Continuous pressure airway pressure (CPAP) does overcome the periods of obstruction and prevents the morbidity associated with obstructive sleep apnea (OSA).  Forty-Six percent of type 1 diabetic patients have absence of effort sleep apnea which means it is a central lack of drive to breath.  There is evidence of change of structure in the medulla of subjects with type 1 diabetes as well as evidence of injuries in the medulla that cause cessation of breathing.  These observations indicate that central neuropathy caused by hyperglycemia does cause central sleep apnea and possibly death.

Enrique C. Morales-Villegas1, Luis A. Alcocer-Diaz-Barreiro2, Gualberto Moreno-Virgen1

1 Cardiometabolic Research Center-MAC Hospital. Aguascalientes, México.
2Mexican Institute of Cardiovascular Health.


In patients with hypertension (HT), cardiovascular risk reduction is directly proportional to the reduction in blood pressure sustained over time. However, in “real life,” blood pressure control is often insufficient or not sustained over time to achieve optimal cardiovascular risk reduction. In this article, we comment on the multiple reasons which explain this common therapeutic failure.
Also, in this article, we summarize the amazing basic and clinical phase III evidence of azilsartan (AZL) and azilsartan combined with chlortalidone (CLD), two excellent therapeutic options for HT control. With such evidence as scientific background, we communicate our results with almost 300 HT patients treated with azilsartan and azilsartan/chlortalidone in “real life.” In brief, our findings were the following:
  1. a) In HT patients with blood pressure (BP) <150/90 mmHg, AZL 40 mg as monotherapy provides practically 100% success to achieve a target BP <140/90 and <130/80 mmHg, in a subpopulation that we have called “hyper-responders”
  2. b) In HT patients with BP <150/90 mmHg (naive or with another treatment failure), AZL/CLD 40/12.5 mg provides practically 100% success to achieve a target BP <140/90 mmHg and 90% to achieve a target BP <130/80 mmHg;
  3. c) In HT patients with BP >150/90 mmHg (generally with another treatment failure), AZL/CLD 80/12.5 mg gives women a success rate greater than 60% to achieve a target BP <140/90 mmHg and greater than 50% to achieve a target BP <130/80 mmHg. The success rates were higher in men, greater than 75% to achieve a target BP <140/90 mmHg and greater than 60% to achieve a target BP <130/80 mmHg. In both cases, the use of amlodipine (2.5, 5, or 10 mg) made it possible to achieve a target BP <140/90 mmHg in 100% of the cases and <130/80 mmHg in 80% of the cases.

Finally, according to our results, we propose a simple three-step strategy based on evidence, personalization, and empowerment which allows reaching a target BP <140/90 mmHg in more than 90% of cases and a target BP <130/80 mmHg in more than 75% of cases in 4 to 12 weeks.

Jorge Ruiz-Medrano1,2Lucia Gonzalez-Buendia1,2José M Ruiz-Moreno1,2,3

1Department of Ophthalmology, Puerta de Hierro-Majadahonda University Hospital, Madrid (Spain).
2Instituto de Microcirugía Ocular (IMO). Madrid; VISSUM. Alicante (Spain).
3Department of Ophthalmology, Castilla La Mancha University, Albacete (Spain).


Diabetic macular edema (DME) is the most common cause of vision loss in diabetic patients. Multiple therapeutic options are currently available for these patients, including laser photocoagulation; intravitreal injections of anti-vascular endothelial growth factor (VEGF) drugs or steroids; or pars plana vitrectomy for tractional DME. The initial treatment for DME is well-defined and widely accepted, with anti-VEGF as first-line option. Nevertheless, between 30 and 40% of patients show partial response or no response whatsoever. There is no consensus on the number of injections needed in order to classify a patient as a non-responder or sub-optimal responder, nor on the definition of the latter. In this study, these concepts are analysed as well as the different therapeutic alternatives at hand, with special interest on the switch between different anti-VEGF and/or steroids. These analyses are performed from an anatomical and functional point of view as well as from an economic, cost-effectiveness perspective. Recent evidence suggests that an early switch to dexamethasone implant in eyes that did not respond adequately to anti-VEGF therapy after 3 injections provides better functional outcomes while alleviating the heavy economic burden of this disease.

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