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OBJECTIVE--To test the hypothesis that insulin detemir, which is associated with less weight gain than other basal insulin formulations, exerts its weight-modulating effects by acting on brain regions involved in [...]

OBJECTIVE--To investigate the associations between changes in body composition and fitness after exercise training and changes in hemoglobin [A.sub.1c] ([HbA.sub.1c]) in individuals with type 2 diabetes. RESEARCH DESIGN AND METHODS--Participants [...]

OBJECTIVE--To determine whether adolescents with type 1 diabetes have left ventricular functional changes at rest and during acute exercise and whether these changes are affected by metabolic control and diabetes [...]

OBJECTIVE--To determine the usefulness of measuring hemoglobin [Al.sub.c] (A1C), alone or combined with the fasting glucose test, compared with the oral glucose tolerance test (OGTT) for the reassessment of the [...]

OBJECTIVE--TO assess differences between the effects of aerobic and resistance training on [HbA.sub.1c] (primary outcome) and several metabolic risk factors in subjects with type 2 diabetes, and to identify predictors [...]

The pathobiology of type 2 diabetes (T2D) is heterogeneous and includes alterations in insulin synthesis and target tissue sensitivity. It is commonly accompanied by increased body weight (BW) with associated [...], Fibroblast growth factor 21 (FGF21) mitigates many of the pathogenic features of type 2 diabetes, despite a short circulating haft-life. PEGylation is a proven approach to prolonging the duration of action while enhancing biophysical solubility and stability. However, in the absence of a specific protein PEGylation site, chemical corrugation is inherently heterogeneous and commonly leads to dramatic loss in bioactivity. This work illustrates a novel means of specific PEGylation, producing FGF21 analogs with high specific activity and salutary biological activities. Using homology modeling and structure-based design, specific sites were chosen in human FGF21 for site-specific PEGylation to ensure that receptor binding regions were preserved. The in vitro activity of the PEGylated FGF21 analogs corresponded with the site of PEG placement within the binding model. Site-specific PEGylated analogs demonstrated dramatically increased circulating haft-life and enhanced efficacy in db/db mice. Twice-weekly dosing of an optimal FGF21 analog reduced blood glucose, plasma lipids, liver triglycerides, and plasma glucagon and enhanced pancreatic insulin content, islet number, and glucose-dependent insulin secretion. Restoration of insulin sensitivity was demonstrated by the enhanced ability of insulin to induce Akt/ protein kinase B phosphorylafion in liver, muscle, and adipose tissues. PEGylation of human FGF21 at a specific and preferred site confers superior metabolic pharmacology. Diabetes 61:505-512, 2012

Diabetic retinopathy (DR) is a major complication of diabetes and often leads to severe visual disabilities. Recent studies reveal that chronic inflammation plays a causal role in the development and [...], Inflammation plays an important role in diabetes-induced retinal vascular leakage. The purpose of this study is to examine the role of endoplasmic reticulum (ER) stress and the signaling pathway of ER stress-induced activating transcription factor 4 (ATF4) in the regulation of Muller cell-derived inflammatory mediators in diabetic retinopathy. In diabetic animals, elevated ER stress markers, ATF4, and vascular endothelial growth factor (VEGF) expression were partially localized to Muller cells in the retina. In cultured Muller cells, high glucose induced a time-dependent increase of ER stress, ATF4 expression, and inflammatory factor production. Inducing ER stress or overexpressing ATF4 resulted in elevated intracellular adhesion molecule 1 and VEGF proteins in Muller cells. In contrast, alleviation of ER stress or blockade of ATF4 activity attenuated inflammatory gene expression induced by high glucose or hypoxia. Furthermore, we found that ATF4 regulated the c-Jun N[H.sub.2]-terminal kinase pathway resulting in VEGF upregulation. ATF4 was also required for ER stress-induced and hypoxia-inducible factor-1α activation. Finally, we showed that administration of chemical chaperone 4-phenylbutyrate or genetic inhibition of ATF4 successfully attenuated retinal VEGF expression and reduced vascular leakage in mice with STZ-induced diabetes. Taken together, our data indicate that ER stress and ATF4 play a critical role in retinal inflammatory signaling and Muller cell-derived inflammatory cytokine production in diabetes. Diabetes 61:492-504, 2012

Although the classic view of diabetic nephropathy (DN) has focused on events leading to glomerular dysfunction, the gradual decline of renal function in later stages of DN is invariably associated [...], This study investigated the mechanisms underlying tubular apoptosis in diabetes by identifying proapoptotic genes that are differentially upregulated by reactive oxygen species in renal proximal tubular cells (RPTCs) in models of diabetes. Total RNAs isolated from renal proximal tubules (RPTs) of 20-week-old heterozygous db/m+, db/db, and db/db catalase (CAT)-transgenic (Tg) mice were used for DNA chip microarray analysis. Real-time quantitative PCR assays, immunohistochemistry, and mice rendered diabetic with streptozotocin were used to validate the proapoptotic gene expression in RPTs. Cultured rat RPTCs were used to confirm the apoptotic activity and regulation of proapoptotic gene expression. Additionally, studies in kidney tissues from patients with and without diabetes were used to confirm enhanced proapoptotic gene expression in RPTs. Bcl-2-modifying factor (Bmf) was differentially upregulated (P < 0.01) in RPTs of db/db mice compared with db/m+ and db/db CAT-Tg mice and in RPTs of streptozotocin-induced diabetic mice in which insulin reversed this finding. In vitro, Bmf cDNA overexpression In rat RPTCs coimmunoprecipated with Bcl-2, enhanced caspase-3 activity, and promoted apoptosis. High glucose (25 mmol/L) induced Bmf mRNA expression in RPTCs, whereas rotenone, catalase, diphenylene iodinium, and apocynin decreased it. Knockdown of Bmf with small interfering RNA reduced high glucose-induced apoptosis in RPTCs. More important, enhanced Bmf expression was detected in RPTs of kidneys from patients with diabetes. These data demonstrate differential upregulation of Bmf in diabetic RPTs and suggest a potential role for Bmf in regulating RPTC apoptosis and tubular atrophy in diabetes. Diabetes 61:474-484, 2012

The increased prevalence of type 2 diabetes mellitus (T2DM) has focused attention on the elevated incidence of diabetic atherosclerosis (1). Insulin resistance (IR) is assumed to trigger the developments of [...], Insulin resistance triggers the developments of diabetes mellitus and atherosclerosis. Tribbles homolog 3 (TRIB3) is involved in insulin resistance. We aimed to investigate whether TRIB3 is implicated in diabetic atherosclerosis. Sixty 3-week-old apohpoprotein E ([ApoE.sup.-/-])/LDR receptor ([LDLR.sup.-/-]) mice were randomly divided into chow and diabetes groups. Diabetes was induced by a high-fat and high-sugar diet combined with low-dose streptozotocin. Mice in both groups were randomly divided into vehicle and TRIB3-silencing groups. After transfection, all mice were killed to evaluate the effects of TRIB3 on atherosclerosis. Silence of TRIB3 markedly decreased insulin resistance (P = 0.039) and glucose (P = 0.019), regardless of diabetes. Ultrasonography-measured parameters were similar in both groups, with and without silence of TRIB3. However, silence of TRIB3 decreased the aortic atherosclerotic burden (P = 1 x [10.sup.-13]). Further study showed that in brachiocephalic lesions, fibrous cap thickness, cap-to-core ratio, collagen content, and the number of smooth muscle cells were significantly increased (P < 0.01 for all) by silence of TRIB3, whereas lipid and macrophage contents remained unaltered, with the vulnerability index significantly reduced. Moreover, the numbers of apoptotic cells and macrophages in brachiocephalic lesions were both significantly decreased (P < 0.01 for both). Macrophage migration was decreased (P = 4 x [10.sup.-4]) by knocking down TRIB3, whereas adhesion and phagocytosis were increased (P < 0.05 for both). Silence of TRIB3 would diminish atherosclerotic burden and increase the plaque stability in diabetic mice. Diabetes 61:463-473, 2012

The molecular determinants in the control of initiation, coordination, and perpetuation of innate and adaptive immune responses that together precipitate β-cell destruction and eventual development of clinical type 1 diabetes [...], More than one-half of the -50 human chemokines have been associated with or implicated in the pathogenesis of type 1 diabetes, yet their actual expression patterns in the islet environment of type 1 diabetic patients remain, at present, poorly defined. Here, we have integrated a human islet culture system, murine models of virus-induced and spontaneous type 1 diabetes, and the histopathological examination of pancreata from diabetic organ donors with the goal of providing a foundation for the informed selection of potential therapeutic targets within the chemokine/ receptor family. Chemokine (C-C motif) ligand (CCL) 5 (CCL5), CCL8, CCL22, chemokine (C-X-C motif) ligand (CXCL) 9 (CXCL9), CXCL10, and chemokine (C-X3-C motif) ligand (CX3CL) 1 (CX3CL1) were the major chemokines transcribed (in an inducible nitric oxide synthase-dependent but not nuclear factor-κB-dependent fashion) and translated by human islet cells in response to in vitro inflammatory stimuli. CXCL10 was identified as the dominant chemokine expressed in vivo in the islet environment of prediabetic animals and type 1 diabetic patients, whereas CCL5, CCL8, CXCL9, and CX3CL1 proteins were present at lower levels in the islets of both species. Of importance, additional expression of the same chemokines in human acinar tissues emphasizes an under-appreciated involvement of the exocrine pancreas in the natural course of type 1 diabetes that will require consideration for additional type 1 diabetes pathogenesis and immune intervention studies. Diabetes 61:436-446, 2012

Insulin receptor (InsR) signaling in the central nervous system (1,2) regulates energy balance (3). Inactivation of InsR in neurons and glia ('NIRKO' mice) predisposes to diet-induced obesity (4), whereas intracerebroventricular [...], OBJECTIVE--The sites of insulin action in the central nervous system that regulate glucose metabolism and energy expenditure are incompletely characterized. We have shown that mice with hypothalamic deficiency (L1) of insulin receptors (InsRs) fail to regulate hepatic glucose production (HGP) in response to insulin. RESEARCH DESIGN AND METHODS--To distinguish neurons that mediate insulin's effects on HGP from those that regulate energy homeostasis, we used targeted knock-ins to express InsRs in agouti-related protein (AgRP) or proopiomelanocortin (POMC) neurons of L1 mice. RESULTS--Restoration of insulin action in AgRP neurons normalized insulin suppression of HGP. Surprisingly, POMC-specific InsR knock-in increased energy expenditure and locomotor activity, exacerbated insulin resistance and increased HGP, associated with decreased expression of the ATe-sensitive [K.sup.+] channel (KATe channel) sulfonylurea receptor 1 subunit, and decreased inhibitory synaptic contacts on POMC neurons. CONCLUSIONS--The contrasting phenotypes of InsR knockins in POMC and AgRP neurons suggest a branched-pathway model of hypothalamic insulin signaling in which InsR signaling in AgRP neurons decreases HGP, whereas InsR activation in POMC neurons promotes HGP and activates the melanocortinergic energy expenditure program. Diabetes 59:337-346, 2010

OBJECTIVE--Offspring of obese mothers have an increased risk for obesity and diabetes. The purpose of this study as to determine whether fetuses of obese women have increased obesity, insulin resistance, [...]

Adipose tissue is increasingly viewed as an endocrine organ that secretes many types of adipokines (such as leptin, tumor necrosis factor-α, interleukin 6, and adiponectin) that modulate the action of [...], OBJECTIVES--The mechanisms behind the association between retinol-binding protein-4 (RBP4) and insulin resistance are not well understood. An interaction between iron and vitamin A status, of which RBP4 is a surrogate, has long been recognized. We hypothesized that iron-associated insulin resistance could be behind the impaired insulin action caused by RBP4. RESEARCH DESIGN AND METHODS--Serum ferritin and RBP4 concentration and insulin resistance were evaluated in a sample of middle-aged men (n = 132) and in a replication independent study. Serum RBP4 was also studied before and after iron depletion in patients with type 2 diabetes. Finally, the effect of iron on RBP4 release was evaluated in vitro in adipose tissue. RESULTS--A positive correlation between circulating RBP4 and log serum ferritin (r = 0.35 and r = 0.61, respectively; P < 0.0001) was observed in both independent studies. Serum RBP4 concentration was higher in men than women in parallel to increased ferritin levels. On multiple regression analyses to predict serum RBP4, log serum ferritin contributed significantly to RBP4 variance after controlling for BMI, age, and homeostasis model assessment value. Serum RBP4 concentration decreased after iron depletion in type 2 diabetic patients (percent mean difference -13.7 [95% CI -25.4 to -2.04]; P = 0.024). The iron donor lactoferrin led to increased dose-dependent adipose tissue release of RBP4 (2.4-fold, P = 0.005) and increased RBP4 expression, while apotransferrin and deferoxamine led to decreased RBP4 release. CONCLUSIONS--The relationship between circulating RBP4 and iron stores, both cross-sectional and after iron depletion, and in vitro findings suggest that iron could play a role in the RBP4-insulin resistance relationship.

Type 1 diabetes is an autoimmune disease that results in destruction of the insulin-producing β-cells (1). Cytokines, such as interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α, and interferon-γ/(IFN-γ), induce β-cell death [...], OBJECTIVE--The transcription factor nuclear factor-κB (NFκB) and the mitogen-activated protein kinases (MAPKs) c-Jun N[H.sub.2]-terminal kinase (JNK) 1/2 are known to play decisive roles in cytokine-induced damage of rodent β-cells. The upstream events by which these factors are activated in response to cytokines are, however, uncharacterized. The aim of the present investigation was to elucidate a putative role of the MAPK kinase kinase-1 (MEKK-1) in cytokine-induced signaling. RESEARCH DESIGN AND METHODS--To establish a functional role of MEKK-1, the effects of transient MEKK-1 overexpression in βTC-6 cells, achieved by lipofection and cell sorting, and MEKK-1 downregulation in βTC-6 cells and human islet cells, achieved by diced-small interfering RNA treatment, were studied. RESULTS--We observed that overexpression of wild-type MEKK-1, but not of a kinase dead MEKK-1 mutant, resulted in potentiation of cytokine-induced JNK activation, inhibitor of κB (IκB) degradation, and cell death. Downregulation of MEKK-1 in human islet cells provoked opposite effects, i.e., attenuation of cytokine-induced JNK and MKK4 activation, IκB stability, and a less pronounced NF-κB translocation. βTC-6 cells with a downregulated MEKK-1 expression displayed also a weaker cytokine-induced iNOS expression and lower cell death rates. Also primary mouse islet cells with downregulated MEKK-1 expression were protected against cytokine-induced cell death. CONCLUSIONS--MEKK-1 mediates cytokine-induced JNK- and NF-κB activation, and this event is necessary for iNOS expression and cell death. Diabetes 57:1896-1904, 2008

Defective negative selection caused by weak interactions between serf-peptides and major histocompatibility complex (MHC) molecules has been proposed as a mechanism that may contribute to autoimmunity. We have been interested [...], OBJECTIVE--Weak major histocompatibility complex (MHC) binding of self-peptides has been proposed as a mechanism that may contribute to autoimmunity by allowing for escape of autoreactive T-cells from the thymus. We examined the relationship between the MHC-binding characteristics of a β-cell antigen epitope and T-cell autoreactivity in a model of autoimmune diabetes. RESEARCH DESIGN AND METHODS--The binding of a proinsulin epitope, proinsulin-l(47-64) (PI-1[47-64]), to the MHC class II molecules [I-A.sup.g7] and [I-A.sup.k] was measured using purified class II molecules. T-cell reactivity to the proinsulin epitope was examined in [I-A.sup.g7+] and [I-A.sup.k+] mice. RESULTS--C-peptide epitopes bound very weakly to [I-A.sup.g7] molecules. However, C-peptide-reactive T-cells were induced after immunization in [I-A.sup.g7]-bearing mice (NOD and B6.g7) but not in [I-A.sup.k]-bearing mice (B10.BR and NOD.h4). T-cells reactive with the PI-1(47-64) peptide were found spontaneously in the peripancreatic lymph nodes of pre-diabetic NOD mice. These T-cells were activated by freshly isolated β-cells in the presence of antigen-presenting cells and caused diabetes when transferred into NOD.scid mice. CONCLUSIONS--These data demonstrate an inverse relationship between self-peptide-MHC binding and T-cell autoreactivity for the PI-1(47-64) epitope in autoimmune diabetes.

Programmed death 1 (PD-1) is an immunoreceptor of the CD28/CTLA-4 family whose expression is induced in activated T- and B-cells and in macrophages (1,2). PD-1 has two cytoplasmic tyrosine motifs: [...], OBJECTIVE--Coinhibitory signals mediated via programmed death 1 (PD-1) receptor play a critical role in downregulating immune responses and in maintaining peripheral tolerance. Programmed death 1 ligand 1 (PD-L1), the interacting ligand for PD-1, widely expressed in many cell types, acts as a tissue-specific negative regulator of pathogenic T-cell responses. We investigated the protective potential of PD-L1 on autoimmune diabetes by transgenically overexpressing PD-L1 in pancreatic p-cells in nonobese diabetic (NOD) mice. RESEARCH DESIGN AND METHODS--We established an insulin promoter-driven murine PD-L1 transgenic NOD mouse model to directly evaluate the protective effect of an organ-specific PD-L1 transgene against autoimmune diabetes. Transgene expression, insulitis, and diabetic incidence were characterized in these transgenic NOD mice. Lymphocyte development, Th1 cells, and regulatory T-cells were analyzed in these transgenic mice; and T-cell proliferation, adoptive transfer, and islet transplantation were performed to evaluate the PD-L1 transgene-mediated immuneprotective mechanisms. RESULTS--The severity of insulitis in these transgenic mice is significantly decreased, disease onset is delayed, and the incidence of diabetes is markedly decreased compared with littermate controls. NOD/SCID mice that received lymphocytes from transgenic mice became diabetic at a slower rate than mice receiving control lymphocytes. Moreover, lymphocytes collected from recipients transferred by lymphocytes from transgenic mice revealed less proliferative potential than lymphocytes obtained from control recipients. Transgenic islets transplanted in diabetic recipients survived moderately longer than control islets. CONCLUSIONS--Our results demonstrate the protective potential of transgenic PD-L1 in autoimmune diabetes and illustrate its role in downregulating diabetogenic T-cells in NOD mice. Diabetes 57:1861-1869, 2008

Diabetes is characterized by altered fuel metabolism due to relative or absolute deficiency of insulin. Individuals with uncontrolled diabetes commonly experience hyperphagia (1), which makes glycemic control more difficult. Several [...], AMP-activated protein kinase (AMPK) acts as a cellular energy sensor, being activated during states of low energy charge. Hypothalamic AMPK activity is altered by hormonal and metabolic signals and mediates the feeding response. To determine the effect of diabetes on hypothalamic AMPK activity, we assayed this activity in streptozotocin (STZ)-induced diabetic rats. Compared with control rats, STZ-induced diabetic rats had significant hyperphagia and weight loss. Hypothalamic AMPK phosphorylation and α2-AMPK activity were higher and acetyl-CoA carboxylase activity was lower in diabetic rats than in control rats. Chronic insulin treatment or suppression of hypothalamic AMPK activity completely prevented diabetes-induced changes in food intake as well as in hypothalamic AMPK activity and mRNA expression of neuropeptide Y and proopiomelanocortin. Plasma leptin and insulin levels were profoundly decreased in diabetic rats. Intracerebroventricular administration of leptin and insulin reduced hyperphagia and the enhanced hypothalamic AMPK activity in diabetic rats. These data suggest that leptin and insulin deficiencies in diabetes lead to increased hypothalamic AMPK activity, which contributes to the development of diabetic hyperphagia.

OBJECTIVE--We have already reported that A1C is elevated because of iron deficiency in late pregnancy among nondiabetic pregnant women. This report examined whether the same phenomenon is observed in pregnant [...]

MARGUERITE J. MCNEELY, MD, MPH Occupation Assistant Professor of Medicine at the University of Washington Research Focus Pre-diabetes Outside Interests Hiking, snowshoeing, gardening Research Funding ADA Career Development Award If [...]

By a News Reporter-Staff News Editor at Women's Health Weekly -- New research on Endocrinology and Diabetes is the subject of a report. According to news reporting out of Suwon, [...]

By a News Reporter-Staff News Editor at Obesity, Fitness & Wellness Week -- Investigators discuss new findings in Obesity and Diabetes. According to news reporting from Glasgow, United Kingdom, by [...]

By a News Reporter-Staff News Editor at Obesity, Fitness & Wellness Week -- Researchers detail new data in Type 2 Diabetes Mellitus. According to news reporting from Tubingen, Germany, by [...]

By a News Reporter-Staff News Editor at Obesity, Fitness & Wellness Week -- New research on Weight Loss is the subject of a report. According to news reporting out of [...]

'Raised maternal body mass index (BMI) in association with hyperglycemia is associated with adverse pregnancy outcome. The contribution of raised BMI as an independent risk factor for adverse pregnancy outcome [...]

New investigation results, 'Changes in serum lipids and blood glucose in non diabetic patients with metabolic syndrome after mixed meals of different composition,' are detailed in a study published in [...]

Investigators discuss in 'Interferon gamma (IFN-?) disrupts energy expenditure and metabolic homeostasis by suppressing SIRT1 transcription' new findings in Type 2 Diabetes Mellitus. 'Chronic inflammation impairs metabolic homeostasis and is [...]

'It is now recognized that obesity is driving the type 2 diabetes epidemic in Western countries,' researchers in La Jolla, California report (see also Type 2 Diabetes Mellitus). 'Obesity-associated chronic [...]

According to the authors of recent research published in the journal Biometals, 'Serum proteins exist in a state of higher glycation among individuals with poor glycemic control, notably diabetics. These [...]

'The endoplasmic reticulum (ER) stress response, also commonly known as the unfolded protein response (UPR), is an adaptive response used to align ER functional capacity with demand. It is activated [...]

According to the authors of recent research from Kyoto, Japan, 'Diabetic cardiomyopathy is characterized by energetic dysregulation caused by glucotoxicity, lipotoxicity, and mitochondrial alterations. p53 and its downstream mitochondrial assembly [...]

Researchers detail in 'Leptin receptor signaling supports cancer cell metabolism through suppression of mitochondrial respiration in vivo,' new data in Adipokines. 'Obesity represents a risk factor for certain types of [...]

'Changes in body fat distribution and abnormal glucose metabolism are common in HIV-infected patients. We hypothesized that HIV-infected participants would have a higher prevalence of impaired glucose tolerance (IGT) compared [...]

'Although obesity and type 2 diabetes mellitus are associated with Gram-positive infections and a worse clinical outcome, it is unknown whether adipocytes can be infected by Gram-positive bacteria. Adipocyte-like differentiated [...]

Researchers detail in 'Cellular bioenergetics as a target for obesity therapy,' new data in Obesity. 'Obesity develops when energy intake exceeds energy expenditure. Although most current obesity therapies are focused [...]

'Amylin interacts with leptin to alter metabolism. We evaluated, for the first time, amylin- and/or leptin-activated signaling pathways in human peripheral tissues (hPTs),' researchers in Boston, United States report (see [...]

According to recent research published in the journal Diabetes Obesity & Metabolism, 'The incidence of insulin resistance and metabolic syndrome correlates with the availability of magnesium (Mg). We studied the [...]

According to recent research published in the journal Proceedings of the Nutrition Society, 'Body fat distribution plays an important role in determining metabolic health. Whereas central obesity is closely associated [...]

Data detailed in 'Chemical and immunochemical detection of 8-halogenated deoxyguanosines at early stage inflammation' have been presented. 'Myeloperoxidase (MPO) generates reactive halogenating species that can modify DNA. The aim of [...]

Researchers detail in 'The lipocalins retinol-binding protein-4, lipocalin-2 and lipocalin-type prostaglandin D2-synthase correlate with markers of inflammatory activity, alcohol intake and blood lipids, but not with insulin sensitivity in metabolically [...]

A report, 'Regulation of adiponectin production by insulin: interactions with tumor necrosis factor-a and interleukin-6,' is newly published data in American Journal of Physiology Endocrinology and Metabolism. 'Obesity is often [...]

'Transcriptional peroxisome proliferator-activated receptor-gamma coactivator-1 alpha (PGC-1 alpha) plays a key role in mitochondrial biogenesis and energy metabolism and is suggested to be involved in the exercise-induced increase in mitochondrial [...]

A report, 'Increased bone resorption and impaired bone microarchitecture in short-term and extended high-fat diet-induced obesity,' is newly published data in Metabolism. 'Although obesity traditionally has been considered a condition [...]

According to recent research published in the journal Current Opinion in Endocrinology Diabetes and Obesity, 'Of review Chronic heart failure (CHF) is a common condition with significant morbidity despite optimal [...]

Researchers detail in 'Exercise training reduces insulin resistance and upregulates the mTOR/p70S6k pathway in cardiac muscle of diet-induced obesity rats,' new data in Proinsulin. 'Obesity and insulin resistance are rapidly [...]

Researchers detail in 'Antihyperlipidemic effect of chlorogenic acid and tetrahydrocurcumin in rats subjected to diabetogenic agents,' new data in diabetes. 'Diabetes mellitus is associated with dyslipidemia, which is a significant [...]

Researchers detail in 'Long-term effects of gestational diabetes on offspring health are more pronounced in skeletal growth than body composition and glucose tolerance,' new data in diabetes. 'Infants of diabetic [...]