The number of people diagnosed with diabetes continues to increase, especially among younger populations. Apart from genetic predisposition and lifestyle, there is increasing scientific and public concern that environmental agents may also contribute to diabetes. Food contamination by chemical substances that originate from packaging materials, or are the result of chemical reactions during food processing, is generally recognized as a worldwide problem with potential health hazards. Phthalates, bisphenol A (BPA) and acrylamide (AA) have been the focus of attention in recent years, due to the numerous adverse health effects associated with their exposure. This paper summarizes the available data about the association between phthalates, BPA and AA exposure and diabetes. Although their mechanism of action has not been fully clarified, in vitro, in vivo and epidemiological studies have made significant progress toward identifying the potential roles of phthalates, BPA and AA in diabetes development and progression. These chemicals interfere with multiple signaling pathways involved in glucose and lipid homeostasis and can aggravate the symptoms of diabetes. Especially concerning are the effects of exposure during early stages and the gestational period. Well-designed prospective studies are needed in order to better establish prevention strategies against the harmful effects of these food contaminants.

β-cells convert glucose (input) resulting in the controlled release of insulin (output), which in turn has the role to maintain glucose homeostasis. β-cell function is regulated by a complex interplay between the metabolic processing of the input, its transformation into second-messenger signals, and final mobilization of insulin-containing granules towards secretion of the output. Failure at any level in this process marks β-cell dysfunction in diabetes, thus making β-cells obvious potential targets for therapeutic purposes. Addressing quantitatively β-cell (dys)function at the molecular level in living samples requires probing simultaneously the spatial and temporal dimensions at the proper resolution. To this aim, an increasing amount of research efforts are exploiting the potentiality of biophysical techniques. In particular, using excitation light in the visible/infrared range, a number of optical-microscopy-based approaches have been tailored to the study of β-cell-(dys)function at the molecular level, either in label-free mode (i.e., exploiting intrinsic autofluorescence of cells) or by the use of organic/genetically-encoded fluorescent probes. Here, relevant examples from the literature are reviewed and discussed. Based on this, new potential lines of development in the field are drawn.

Extracellular vesicles (EVs) released by cells throughout the body have been implicated in diabetes pathogenesis. Understanding the role of EVs in regulation of β-cell function and viability may provide insights into diabetes etiology and may lead to the development of more effective screening and diagnostic tools to detect diabetes earlier and prevent disease progression. This review was conducted to determine what is known from the literature about the effect of EV crosstalk on pancreatic β-cell function and viability in the pathogenesis of diabetes mellitus, to perform a gap analysis for future research directions, and to discuss implications of available evidence for diabetes care. The literature search yielded 380 studies from which 31 studies were determined to meet eligibility criteria. The majority of studies had the disease context of autoimmunity in T1DM. The most commonly studied EV crosstalk dynamics involved localized EV-mediated communication between β-cells and other islet cells, or between β-cells and immune cells. Other organs and tissues secreting EVs that affect β-cells include skeletal muscle, hepatocytes, adipocytes, immune cells, bone marrow, vascular endothelium, and mesenchymal stem cells. Characterization of EV cargo molecules with regulatory effects in β-cells was conducted in 24 studies, with primary focus on microRNA cargo. Gaps identified included scarcity of evidence for the effect on β-cell function and viability of EVs from major metabolic organs/tissues such as muscle, liver, and adipose depots. Future research should address these gaps as well as characterize a broader range of EV cargo molecules and their activity in β-cells.

BACKGROUND: Type 2 diabetes is the most common type of diabetes and its prevalence is rapidly increasing throughout the world. Modifications of lifestyle such as suitable diet and exercise programs along with pharmacotherapy and education of patients are beneficial therapies for patients with type 2 diabetes. The ethnopharmacological use of herbal medicines, many of them part of our diet as spices, vegetables and fruits, has been developed for the treatment of diabetes due to inexpensiveness, easy availability and few side effects.
OBJECTIVE: Our aim is to present a review for researchers who are interested in the biologically active dietary plants traditionally utilized in the treatment of diabetes.
METHODS: Information was obtained from a literature search of electronic databases such as Google Scholar, Pubmed, Sci Finder and Cochrane. Common and scientific name of the fruits, vegetables, beverages, oils and spices and the words \'antidiabetic\', \'hypoglycemic\', \'anti-hyperglycemic\', \'type 2 diabetes\' were used as keywords for search.
RESULTS: Certain fruits and vegetables are functional foods and their consumption reduces the incidence of type 2 diabetes. Hypoglycemic effects of fruits and vegetables may be due to their inducing nature on pancreatic β-cells for insulin secretion, or bioactive compounds such as flavonoids, alkaloids and anthocyanins, which act as insulin-like molecules or insulin secretagogues.
CONCLUSIONS: This write-up covers hypoglycemic, anti-hyperglycemic and anti-diabetic activities of some dietary fruits, vegetables, beverages, oils and spices and their active hypoglycemic constituents. Including such plant species in the diet might improve management of type 2 diabetes.

The PPAR-γ receptor agonists, as a relatively new and perhaps still not very widely used class of antidiabetic agent in the Caribbean and particularly the Trinidadian context, possess pharmacologic properties that certainly have been shown to have impact on many of the inflammatory, metabolic, biochemical and structural macrovascular aberrations that occur in the type 2 diabetic. Activation of PPAR(gamma) nuclear receptors regulates the transcription of insulin-responsive genes involved in the control of glucose production, transport, and utilization. PPAR(gamma)-responsive genes also participate in the regulation of fatty acid metabolism, an important contributory pathogenic factor in this subset of patients. The unique mode of action of this class of therapeutic agent addresses a range of anomalies occurring at the cellular and sub-cellular level that are injurious to the diabetic. My aim in addressing the issue of the potential impact of PPAR-γ receptor agonists on cardiovascular disease (CVD) morbidity and mortality in the diabetic, is first, to seek to enhance both an awareness of, and greater familiarity among our own physicians, with this class of drug, and secondly, to effect a timely review of the recent literature as it relates to the tremendous possibilities for the potential clinical gains that might accrue from their use, in so far as this may serve to ameliorate the ravages of the CVD disease that all too tragically attends the type 2 diabetic, and more specifically those with the insulin resistance syndrome. (Mol Cell Biochem 263: 189-210, 2004).

Mathematical modeling of the electrical activity of the pancreatic β-cell has been extremely important for understanding the cellular mechanisms involved in glucose-stimulated insulin secretion. Several models have been proposed over the last 30 y, growing in complexity as experimental evidence of the cellular mechanisms involved has become available. Almost all the models have been developed based on experimental data from rodents. However, given the many important differences between species, models of human β-cells have recently been developed. This review summarizes how modeling of β-cells has evolved, highlighting the proposed physiological mechanisms underlying β-cell electrical activity.