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Several strategies are available to address the obesity epidemic and range from noninvasive lifestyle interventions to medications and bariatric surgical procedures. Endoscopic bariatric techniques, such as intragastric balloons, have become an attractive alternative as a tool for weight loss that can augment the effect of lifestyle interventions. This technical review includes multiple systematic reviews performed to support a clinical practice guideline by the American Gastroenterological Association on the role of intragastric balloons as a tool for weight loss. The systematic reviews targeted a priori selected clinical questions about the effectiveness and periprocedural care of intragastric balloons and concomitant and subsequent weight-loss strategies.Diabetes is one of the most prevalent metabolic diseases and its incidence is increasing throughout the world. Data from World Health Organization (WHO) point-out that diabetes is a major cause of blindness, kidney failure, heart attacks, stroke and lower limb amputation and estimated 1.6 million deaths were directly caused by it in 2016. Population studies show that the incidence of this disease increases in women after menopause, when the production of estrogen is decreasing in them. Knowing the impact that estrogenic signaling has on insulin-secreting β cells is key to prevention and design of new therapeutic targets. This chapter explores the role of estrogen and their receptors in the regulation of insulin secretion and biosynthesis, proliferation, regeneration and survival in pancreatic β cells. this website In addition, delves into the genetic animal models developed and its application for the specific study of the different estrogen signaling pathways. Finally, discusses the impact of menopause and hormone replacement therapy on pancreatic β cell function.Type 2 diabetes (T2D), a heterogeneous disorder derived from metabolic dysfunctions, leads to a glucose overflow in the circulation due to both defective insulin secretion and peripheral insulin resistance. One of the critical risk factor for T2D is obesity, which represents a global epidemic that has nearly tripled since 1975. Obesity is characterized by chronically elevated free fatty acid (FFA) levels, which cause deleterious effects on glucose homeostasis referred to as lipotoxicity. Here, we review the physiological FFA roles onto glucose-stimulated insulin secretion (GSIS) and the pathological ones affecting many steps of the mechanisms and modulation of GSIS. We also describe in vitro and in vivo experimental evidences addressing lipotoxicity in β-cells and the role of saturation and chain length of FFA on the potency of GSIS stimulation. The molecular mechanisms underpinning lipotoxic-β-cell dysfunction are also reviewed. Among them, endoplasmic reticulum stress, oxidative stress and mitochondrial dysfunction, inflammation, impaired autophagy and β-cell dedifferentiation. Finally therapeutic strategies for the β-cells dysfunctions such as the use of metformin, glucagon-like peptide 1, thiazolidinediones, anti-inflammatory drugs, chemical chaperones and weight are discussed.Long non-coding RNAs (lncRNAs) are transcripts of more than 200 nucleotides that have not coding potential, but act as gene expression regulators through several molecular mechanisms. Several studies have identified tons of lncRNAs that are expressed in pancreatic β cells and many of them have been shown to have β cell-specific expression, suggesting a potential role in the regulation of basal β cell functions. Indeed, accumulating evidence based on numerous studies, has highlighted the implication of lncRNAs in the regulation of pancreatic β cell differentiation and proliferation, insulin synthesis and secretion, and apoptosis. In addition, several lncRNAs have shown to be implicated in pancreatic β cell dysfunction linked to different types of diabetes, including type 1 and type 2 diabetes, and monogenic forms of the disease. Pathogenic conditions linked to diabetes (inflammation or lipoglucotoxicity, for example) dysregulate the expression of several lncRNAs, suggesting that changes in lncRNA may alter potentially important pathways for β cell function, and eventually leading to β cell dysfunction and diabetes development. In this sense, functional characterization of some lncRNAs has demonstrated that these non-coding molecules participate in the regulation of several crucial pathways at the pancreatic β cell level, and dysregulation of these pathways leads to pathogenic phenotypes. In this review, we provide an overview of the action mechanisms of functionally characterized lncRNAs in healthy β cells and describe the contribution of some diabetes-associated lncRNAs to pancreatic β cell failure.The human and mouse islet of Langerhans is an endocrine organ composed of five different cells types; insulin-secreting β-cells, glucagon-producing α-cells, somatostatin-producing δ-cells, pancreatic polypeptide-secreting PP cells and ɛ-cells that secretes ghrelin. The most important cells are the pancreatic β-cells that comprise around 45-50% of human islets and 75-80% in the mouse. Pancreatic β-cells secrete insulin at high glucose concentration, thereby finely regulating glycaemia by the hypoglycaemic effects of this hormone. Different ion channels are implicated in the stimulus-secretion coupling of insulin. An increase in the intracellular ATP concentration leads to closure KATP channels, depolarizing the cell and opening voltage-gated calcium channels. The increase of intracellular calcium concentration induced by calcium entry through voltage-gated calcium channels promotes insulin secretion. Here, we briefly describe the diversity of ion channels present in pancreatic β-cells and the different mechanisms that are responsible to induce insulin secretion in human and mouse cells. Moreover, we described the pathophysiology due to alterations in the physiology of the main ion channels present in pancreatic β-cell and its implication to predispose metabolic disorders as type 2 diabetes mellitus.MicroRNA (miRNAs) are small non-coding RNA involved in gene expression regulation. Emerging evidences identify miRNAs as key regulators of beta cell physiology. Their role in fine-tuned gene expression regulation is crucial in the differentiation of insulin-producing cells and contributes to the acquisition and management of their unique phenotype. Dysregulation of miRNA expression causes beta cell dysfunction and promotes the development of different forms of diabetes mellitus.