GPR162 is a beta cell CART receptor.

Cocaine and amphetamine-regulated transcript (CART) is expressed in pancreatic islet cells and neuronal elements. We have previously established insulinotropic actions of CART in human and rodent islets. The receptor for CART in the pancreatic beta cells is unidentified.

Overexpressed beta cell CART increases insulin secretion in mouse models of insulin resistance and diabetes.

Impaired beta cell function and beta cell death are key features of type 2 diabetes (T2D). Cocaine- and amphetamine-regulated transcript (CART) is necessary for normal islet function in mice. CART increases glucose-stimulated insulin secretion in vivo in mice and in vitro in human islets and CART protects beta cells against glucotoxicity-induced cell death in vitro in rats.

The role of CART in islet biology.

Cocaine- and amphetamine-regulated transcript (CART) is mostly known for its appetite regulating effects in the central nervous system. However, CART is also highly expressed in the peripheral nervous system as well as in certain endocrine cells. Our group has dedicated more than 20 years to understand the role of CART in the pancreatic islets and in this review we summarize what is known to date about CART expression and function in the islets.

SCRT1 is a novel beta cell transcription factor with insulin regulatory properties.

Here we show that scratch family transcriptional repressor 1 (SCRT1), a zinc finger transcriptional regulator, is a novel regulator of beta cell function. SCRT1 was found to be expressed in beta cells in rodent and human islets. In human islets, expression of SCRT1 correlated with insulin secretion capacity and the expression of the insulin (INS) gene.

GK-rats respond to gastric bypass surgery with improved glycemia despite unaffected insulin secretion and beta cell mass.

Roux-en-Y gastric bypass (RYGB) is the most effective treatment for morbid obesity and results in rapid remission of type 2 diabetes (T2D), before significant weight loss occurs. The underlying mechanisms for T2D remission are not fully understood. To gain insight into these mechanisms we used RYGB-operated diabetic GK-rats and Wistar control rats.

Ghrelin suppresses insulin secretion in human islets and type 2 diabetes patients have diminished islet ghrelin cell number and lower plasma ghrelin levels.

It is not known how ghrelin affects insulin secretion in human islets from patients with type 2 diabetes (T2D) or whether islet ghrelin expression or circulating ghrelin levels are altered in T2D. Here we sought out to identify the effect of ghrelin on insulin secretion in human islets and the impact of T2D on circulating ghrelin levels and on islet ghrelin cells. The effect of ghrelin on insulin secretion was assessed in human T2D and non-T2D islets.

Intestinal CART is a regulator of GIP and GLP-1 secretion and expression.

Impaired incretin effect is a culprit in Type 2 Diabetes. Cocaine- and amphetamine-regulated transcript (CART) is a regulatory peptide controlling pancreatic islet hormone secretion and beta-cell survival. Here we studied the potential expression of CART in enteroendocrine cells and examined the role of CART as a regulator of incretin secretion and expression.

Glutamine-Elicited Secretion of Glucagon-Like Peptide 1 Is Governed by an Activated Glutamate Dehydrogenase.

Glucagon-like peptide 1 (GLP-1), secreted from intestinal L cells, glucose dependently stimulates insulin secretion from β-cells. This glucose dependence prevents hypoglycemia, rendering GLP-1 analogs a useful and safe treatment modality in type 2 diabetes. Although the amino acid glutamine is a potent elicitor of GLP-1 secretion, the responsible mechanism remains unclear.

Ghrelin rescues skeletal muscle catabolic profile in the R6/2 mouse model of Huntington's disease.

Accumulating evidence suggests altered energy metabolism as a key feature in Huntington's disease (HD) pathology. Hyper-catabolism, including weight loss and muscle atrophy, is seen in HD patients and HD mouse models. Metabolic hormones are key players, not only in energy metabolism, but also in neurodegenerative processes.

Ghrelin Is a Regulator of Glucagon-Like Peptide 1 Secretion and Transcription in Mice.

The gut hormones ghrelin, glucagon-like peptide 1 (GLP-1), and glucose-dependent insulinotropic peptide (GIP) have been intensively studied for their role in metabolism. It is, however, not well known whether the hormones interplay and regulate the secretion of each other. In this study, we studied the effect of ghrelin on GLP-1, GIP, and insulin secretion during an oral glucose tolerance test (OGTT) in mice.

Endogenous beta-cell CART regulates insulin secretion and transcription of beta-cell genes.

Impaired beta-cell function is key to the development of type 2 diabetes. Cocaine- and amphetamine-regulated transcript (CART) is an islet peptide with insulinotropic and glucagonostatic properties. Here we studied the role of endogenous CART in beta-cell function.

CART is overexpressed in human type 2 diabetic islets and inhibits glucagon secretion and increases insulin secretion.

Aims/hypothesis: Insufficient insulin release and hyperglucagonaemia are culprits in type 2 diabetes. Cocaine- and amphetamine-regulated transcript (CART, encoded by Cartpt) affects islet hormone secretion and beta cell survival in vitro in rats, and Cart (-/-) mice have diminished insulin secretion. We aimed to test if CART is differentially regulated in human type 2 diabetic islets and if CART affects insulin and glucagon secretion in vitro in humans and in vivo in mice.

Increased Melatonin Signaling Is a Risk Factor for Type 2 Diabetes.

Type 2 diabetes (T2D) is a global pandemic. Genome-wide association studies (GWASs) have identified >100 genetic variants associated with the disease, including a common variant in the melatonin receptor 1 b gene (MTNR1B). Here, we demonstrate increased MTNR1B expression in human islets from risk G-allele carriers, which likely leads to a reduction in insulin release, increasing T2D risk.

HMGB1 binds to the rs7903146 locus in TCF7L2 in human pancreatic islets.

The intronic SNP rs7903146 in the T-cell factor 7-like 2 gene (TCF7L2) is the common genetic variant most highly associated with Type 2 diabetes known to date. The risk T-allele is located in an open chromatin region specific to human pancreatic islets of Langerhans, thereby accessible for binding of regulatory proteins. The risk T-allele locus exhibits stronger enhancer activity compared to the non-risk C-allele.

[Operation and interaction peculiarities of diagnostic laboratories involved in providing protection from infectious diseases during the XXII Olympic Winter Games and XI Paralympic Winter Games 2014 in Sochi].

The experience of the organization and functioning of the laboratory network during the XXII Olympic Winter Games and XI Paralympic Winter Games of 2014 in Sochi is considered. Efforts to establish an effective system of laboratory support, the order of work and interaction of diagnostic laboratories involved in diseases control of population during the Olympic Games are analyzed.

[Enterovirus non-poliomyelitis infections in Krasnodar region].

Aim: Evaluation of epidemic situation by non-poliomyelitis enterovirus infections in Krasnodar region in multi-year dynamics and characterization of clinical course of enterovirus serous meningitis in hospitalize patients.

Materials And Methods: Retrospective analysis of non-poliomyelitis enterovirus infection epidemi process manifestations during 2002-2012 in Krasnodar region territory based on data of Center of Hygien and Epidemiology in Krasnodar Region.

Results: Clinical-epidemiologic characteristics of enterovirus infections in Krasnodar region are presented.

The role of PI3K/AKT-related PIP5K1α and the discovery of its selective inhibitor for treatment of advanced prostate cancer.

Nitrogen-containing heterocyclic compounds are an important class of molecules that are commonly used for the synthesis of candidate drugs. Phosphatidylinositol-4-phosphate 5-kinase-α (PIP5Kα) is a lipid kinase, similar to PI3K. However, the role of PIP5K1α in oncogenic processes and the development of inhibitors that selectively target PIP5K1α have not been reported.

TCF7L2 is a master regulator of insulin production and processing.

Genome-wide association studies have revealed >60 loci associated with type 2 diabetes (T2D), but the underlying causal variants and functional mechanisms remain largely elusive. Although variants in TCF7L2 confer the strongest risk of T2D among common variants by presumed effects on islet function, the molecular mechanisms are not yet well understood. Using RNA-sequencing, we have identified a TCF7L2-regulated transcriptional network responsible for its effect on insulin secretion in rodent and human pancreatic islets.

Cocaine- and amphetamine-regulated transcript is expressed in adipocytes and regulate lipid- and glucose homeostasis.

Cocaine- and amphetamine-regulated transcript (CART) is a regulatory peptide expressed in the nervous system and in endocrine cells, e.g. in pancreatic islets.

Expression of cocaine- and amphetamine-regulated transcript is associated with worse survival in small bowel carcinoid tumors.

Purpose: Cocaine- and amphetamine-regulated transcript (CART) peptide exerts several regulatory functions acting both as neurotransmitter and hormone. We recently showed that CART is expressed in various neuroendocrine tumors, including small bowel carcinoids. The main objective of the present study was to examine whether CART expression is associated with survival in patients with small bowel carcinoid.

Clinical trial update and novel therapeutic approaches for metastatic prostate cancer.

Recurrent prostate cancer (PCa) remains a major clinical challenge. Invasive and metastatic PCa lesions often exhibit a partial and time-limited response to therapy before the cancer progresses and the patient succumbs to the disease. Despite recent advances in early diagnosis and treatment, approximately one-third of treated patients will relapse and become resistant to currently available treatments.

[The function of membrane Ca-ATPases and nonenzymatic peroxidation of membrane lipids in patients with hypertension].

Alterations in activity of membrane-bound Ca2(+)-ATPases were shown to depend on the rate of lipid peroxidation in cell membranes of patients with hypertension during the period of crisis. On the basis from these results antioxidants and Ca2(+)-antagonistic drugs could be used for treatment of hypertensive crisis. Monitoring of the disease is possible by means of estimation of the membrane-bound Ca2(+)-ATPases activity.