Adipose Tissue-derived Hormone Research Articles

Changes in acyl ghrelin, insulin and leptin of young obese Indonesians following a 4-weeks weight loss program

Changes in acyl ghrelin, insulin and leptin of young obese Indonesians following a 4-weeks weight loss program

Hypothalamic Integration of the Endocrine Signaling Related to Food Intake.

Hypothalamic integration of gastrointestinal and adipose tissue-derived hormones serves as a key element of neuroendocrine control of food intake. Leptin, adiponectin, oleoylethanolamide, cholecystokinin, and ghrelin, to name a few, are in a constant "cross talk" with the feeding-related brain circuits that encompass hypothalamic populations synthesizing anorexigens (melanocortins, CART, oxytocin) and orexigens (Agouti-related protein, neuropeptide Y, orexins). While this integrated neuroendocrine circuit successfully ensures that enough energy is acquired, it does not seem to be equally efficient in preventing excessive energy intake, especially in the obesogenic environment in which highly caloric and palatable food is constantly available. The current review presents an overview of intricate mechanisms underlying hypothalamic integration of energy balance-related peripheral endocrine input. We discuss vulnerabilities and maladaptive neuroregulatory processes, including changes in hypothalamic neuronal plasticity that propel overeating despite negative consequences.

Anti-hypertriglyceridemic Activity of Cornus Mas in Diabetic Rats

Introduction: Hypertriglyceridemia is among the multiple metabolic derangements seen in diabetes mellitus. Cornelian cherry (Cornus mas L.), belongs to the family Cornacea and has been shown to be helpful in treating hyperlipidemia. Aim: The study investigates mechanisms of action of dietary Cornelian Cherry fruit Dried Powder (CCDP) for ameliorating hypertriglyceridemia in diabetic rats. Materials and Methods: An experimental study with parallel controls was performed. Fifty six male adult rats were randomly assigned into 8 equal groups and treated as follows for 4 weeks. Negative control: Normal rats, basic diet; positive control: streptozotocin-induced diabetic rats, basic diet; T1 to T4 groups: diabetic rats fed with diets containing 0.25, 0.5, 1 and 2 g/ 100 g BW CCDP, respectively; T5: diabetic rats fed with basic diet plus 100 mg/kg BW of fenofibrate in drinking water and T6: normal rats fed with basic diet containing 1 g/100 g BW CCDP. Selected serum biochemical parameters, Lipoprotein Lipase (LPL) level as well as Adipose Tissue Hormone Sensitive Lipase (HSL) and Hepatic Peroxisome Proliferator-Activated Receptor Alpha (PPARα) levels were assayed. Analysis of data was performed by one-way ANOVA followed by Tukey’s test with p<0.05 as the significant level. Results: Treatment with CCDP at all dosages as well as fenofibrate decreased serum triglycerides and VLDL levels as compared to positive control. Serum AST significantly decreased in T1, T3 and T4 groups as compared to positive control rats. Serum LPL levels in the diabetic positive control group decreased significantly as compared to negative control. Rats in T1, T2, T4 and T5 groups showed increased serum LPL levels as compared to positive control. No significant difference was observed in hepatic PPARα levels among CCDP-treated and negative or positive controls. Positive control rats showed a significant decrease in adipose tissue HSL levels. Administration of CCDP in T3 group significantly increased HSL values as compared to positive control. CCDP in healthy rats did not change any of these parameters. Conclusion: Findings of the present study confirms positive effects of C. mas fruit on some liver function enzymes and hypertriglyceridemia and clarifies that increased serum LPL levels is at least partly responsible for hypotriglyceridemic effect of the fruit in rats with STZ-induced diabetes mellitus.

Important role of fat tissue hormones in development of comorbid chronic pancreatitis and obesity

Aim of this paper is to consider the role of hormones of the adipose tissue in mechanisms of obesity, metabolic syndrome, type 2 diabetes mellitus upon chronic pancreatitis.&#x0D; Materials and methods. The literature review indicates the value of visceral fat in the development of insulin resistance, dyslipidemia, including atherogenic one, taking into account the possible infiltration of pancreatic tissue by adipocytes. Participation of some adipocytokines of adipose tissue in the development of obesity upon chronic pancreatitis is highlighted. It is shown that in some cases the hormones of visceral adipose tissue, penetrating through the portal vein to the liver and then to the pancreas, aggravated the course of systemic chronic inflammation of the inherent chronic pancreatitis, promote steatosis and development of fatty pancreatic disease.&#x0D; Conclusion. Literary sources indicate the leading role of visceral adipose tissue and its hormones in the formation of obesity in chronic pancreatitis. Due to the infiltration of the pancreatic tissue by adipocytes, lipoidosis and steatosis develop. With the progression of the process type 2 diabetes mellitus, fatty liver or pancreatic disease, or cancer of these orhans. Consequently, there is a need for serious differentiated preventive and curative measures aimed at promoting a healthy lifestyle to improve the quality of life of patients suffering from chronic pancreatitis.

Association Between Peripheral Adipokines and Inflammation Markers: A Systematic Review and Meta-Analysis.

Obesity-induced inflammation potentially promotes a variety of chronic conditions. This study aimed to summarize cross-sectional associations between adipose tissue-derived hormones (leptin and adiponectin) and inflammatory biomarkers (C-reactive protein [CRP], interleukin [IL]-6, and tumor necrosis factor [TNF]-α) by means of meta-analysis. A systematic search of the databases EMBASE and MEDLINE (PubMed) up to January 2017 was conducted. Data were independently extracted and evaluated by two reviewers. Pooled effect sizes and 95% confidence intervals were calculated using random-effects models. After the initial search, 5,907 publications were retrieved; of these, an overall 60 studies with 45,210 participants were deemed eligible for inclusion in the meta-analysis. Positive correlations with inflammatory biomarkers were observed for leptin (pooled Rho = 0.35, 0.20, and 0.20 for CRP, IL-6, and TNF-α, respectively), whereas the respective correlations with adiponectin were negative (pooled Rho = -0.18, -0.14, and -0.12 for CRP, IL-6, and TNF-α, respectively). Stratification by age showed that the observed correlations tended to be weaker with the increasing age of participants. No apparent differences were observed by sex and adiposity status. This is the first quantitative synthesis of human studies on the association between circulating adipokines and inflammation biomarkers. Potential influence of age on these associations requires further evaluation.

Central injection of a synthetic chicken partial leptin peptide does not affect food intake in chicks.

Leptin is an adipose tissue-derived hormone in mammals that plays an important role in whole body energy balance via its inhibitory effects on food intake mediated through the hypothalamus. Chicken leptin has a low sequence homology to mammalian leptin and its role in appetite regulation is not reported; hence the objective of this study was to determine effects of central injection of chicken leptin on food and water intake and associated behaviors in chicks. Chicks were intracerebroventricularly injected with 0 (vehicle), 0.3, 1.0, or 3.0 nmol of a synthetic chicken leptin partial peptide and food and water intake were monitored. There were no effects observed and a second experiment was conducted to evaluate food and water intake at higher doses; after injection of 0, 2.5, 5.0, or 10.0 nmol leptin. Again, there were no effects on food or water intake. In the third experiment, behaviors were analyzed during the first 30 min post-injection of vehicle or 10 nmol leptin. At 5 min post-injection, vehicle-injected chicks spent more time sitting than leptin-injected chicks. A wide dose range was evaluated however, the absence of an effect on food intake or behavior suggests that the chicken leptin peptide that was tested does not mediate effects on appetite in the brain and that chicken leptin likely has a different physiological role in birds than in mammals.

The good and the bad collagens of fibrosis - Their role in signaling and organ function.

Usually the dense extracellular structure in fibrotic tissues is described as extracellular matrix (ECM) or simply as collagen. However, fibrosis is not just fibrosis, which is already exemplified by the variant morphological characteristics of fibrosis due to viral versus cholestatic, autoimmune or toxic liver injury, with reticular, chicken wire and bridging fibrosis. Importantly, the overall composition of the ECM, especially the relative amounts of the many types of collagens, which represent the most abundant ECM molecules and which centrally modulate cellular functions and physiological processes, changes dramatically during fibrosis progression. We hypothesize that there are good and bad collagens in fibrosis and that a change of location alone may change the function from good to bad. Whereas basement membrane collagen type IV anchors epithelial and other cells in a polarized manner, the interstitial fibroblast collagens type I and III do not provide directional information. In addition, feedback loops from biologically active degradation products of some collagens are examples of the importance of having the right collagen at the right place and at the right time controlling cell function, proliferation, matrix production and fate. Examples are the interstitial collagen type VI and basement membrane collagen type XVIII. Their carboxyterminal propeptides serve as an adipose tissue hormone, endotrophin, and as a regulator of angiogenesis, endostatin, respectively. We provide an overview of the 28 known collagen types and propose that the molecular composition of the ECM in fibrosis needs careful attention to assess its impact on organ function and its potential to progress or reverse. Consequently, to adequately assess fibrosis and to design optimal antifibrotic therapies, we need to dissect the molecular entity of fibrosis for the molecular composition and spatial distribution of collagens and the associated ECM.

Metabolic disorders in adipocytokine imbalance and gestational complications

Adipose tissue as an endocrine organ synthesizes a large number of biologically active substances, adipocytokines, which have both local and systemic effects influencing the vascular wall, tissue sensitivity to insulin, glucose metabolism, and systemic inflammation. The data obtained from clinical and experimental studies demonstrate the close relationship between the imbalance of adipocytokines and pregnancy complications such as insulin resistance, gestational diabetes, and preeclampsia. In this connection, close attention of obstetrician-gynecologists and endocrinologists is focused on etiopathogenic aspects of the formation of gestational complications with metabolic disorders caused by an imbalance of adipocytokines with maternal obesity and to the search for markers of these disorders. The review presents the current literature data on adipose tissue hormones and their influence on the course of a gestational process.

Serum apelin levels and metabolic risk markers in obese women

BackgroundAdipose tissue hormones, Adipokines, play an important role in obesity-associated complications. Apelin has recently been added to the family of adipokines. The aim of this study was to evaluate the relationship between serum apelin levels and metabolic abnormal parameters in Egyptian obese women.Materials and methodsThe study included 400 unrelated women; they were 200 obese women and 200 non- obese matched healthy women. All participants underwent clinical, anthropometric and biochemical examinations. Insulin resistance (IR) was determined by the homeostasis model assessment of insulin resistance (HOMA-IR). Serum apelin levels and obesity biomarkers were measured using enzyme-linked immunoassay (ELISA) kits. Fat mass was measured by Tanita Body Composition Analyzer.ResultsObese women showed significant higher levels of serum apelin, leptin, triglycerides, LDL-C, total cholesterol, fasting insulin HOMA-IR and blood pressure levels than controls. Significant positive correlations between apelin and leptin levels with abnormal metabolic markers were noted in obese women.ConclusionThe present study suggests the significant role that might be mediated by apelin for developing abnormal metabolic parameters among Egyptian obese women.

The Anti-Obesity Potential of Green Tea: The Effect on Leptin and Adiponectin

Green tea has been consumed for thousands of years, and has been known to have many medicinal properties such as, anti-cancerous, anti-atherogenic, anti-oxidative, anti-inflammatory and anti-bacterial. With the increasing emergence of cardiovascular disease (CVD), and its major risk factor, obesity, there has been increasing interest in green tea as a potential anti-obesity therapy. Evidence has demonstrated that green tea decreases body weight. However it remains unclear through which pathway and mechanism green tea exerts its anti-obesity properties. The metabolic adipose tissue hormones, adipocytokines, leptin and adiponectin have been studied extensively as a potential target for green tea and its main catechin, epigallacatechin gallate (EGCG). It has been demonstrated that green tea consumption decreases leptin levels which may directly decrease body weight through increasing energy expenditure and fat oxidation. Furthermore, ingestion of green tea or its catechins has been associated with increased adiponectin levels which may indirectly reduce body weight through insulin sensitivity.

Progranulin, a New Adipokine at the Crossroads of Metabolic Syndrome, Diabetes, Dyslipidemia and Hypertension.

Progranulin is a multifunctional regulatory protein with growth-promoting, neuroprotective and antiinflammatory activities. Recent studies indicate that progranulin is one of the adipose tissue hormones (adipokines). Progranulin expression in visceral adipose tissue and circulating progranulin concentration are increased in obesity and hyperprogranulinemia is involved in the pathogenesis of obesity-associated insulin resistance. Progranulin impairs insulin signaling and reduces insulin-induced glucose uptake both in vitro and in vivo whereas progranulin deficiency protects from high fat diet-induced insulin resistance. Several studies, including some prospective ones, have demonstrated the association between high progranulin and type 2 diabetes and its complications such as nephro- and retinopathy as well as non-alcoholic fatty liver disease. It is quite well established that progranulin contributes to insulin resistance and resulting deterioration of carbohydrate metabolism. In addition, progranulin may be associated with the development of diabetic microangiopathy, fatty liver disease and possibly with the increased risk of cancer in subjects with the metabolic syndrome. On the other hand, progranulin augments vasorelaxation, inhibits inflammatory reaction, is neuroprotective and reduces ischemiareperfusion injury. Progranulin has both detrimental and beneficial effects. More clinical studies including prospective ones are needed to clarify the role of progranulin in obesity-associated pathologies such as diabetes, hyperlipidemia, hypertension and atherosclerosis.

A Longitudinal Study of the Relationships Between Mood Symptoms, Body Mass Index, and Serum Adipokines in Bipolar Disorder.

There is a bidirectional relationship between obesity and mood disorders, with each increasing the risk of developing the other. This relationship suggests that they have overlapping pathophysiologic mechanisms. Adipose tissue-derived hormones, or adipokines, regulate appetite and metabolism and have activity in limbic brain regions, making them potential shared etiologic factors between elevated body mass index (BMI) and mood disorders. However, the precise relationships between BMI, mood, and adipokines are unknown. We measured the serum levels of adiponectin, lipocalin-2, resistin, adipsin, and leptin in 53 people with early-stage DSM-IV-defined bipolar disorder, diagnosed with the Mini-International Neuropsychiatric Interview, and 22 healthy comparison subjects. Participants were followed at the University of British Columbia Mood Disorders Centre between June 2004 and June 2012. We were primarily interested in determining, in patients, (1) whether BMI and recent mood episodes predicted adipokine levels and (2) whether adipokine levels in turn predicted subsequent mood relapses and change in BMI. Using linear regression, we found that (1) past-6-month mood episodes predicted lower adiponectin (β = -0.385, P = .04) and adipsin (β = -0.376, P = .03) levels and higher lipocalin-2 levels (β = 0.411, P = .03), (2) BMI did not predict adipokine levels, and (3) treatment with second-generation antipsychotics was associated with higher resistin levels (β = 0.482, P < .01). Furthermore, lower adiponectin (β = -0.353, P = .01) and leptin (β = -0.332, P = .02) levels predicted depressive relapse over 12 months, while higher adipsin (β = 0.496, P < .01) and leptin (β = 0.421, P < .01) levels predicted BMI gain. Our results suggest that mood episodes and medication treatment contribute to adipokine abnormalities in bipolar disorder and that adipokines influence psychiatric illness course and BMI change. Adipokines may represent a novel pathophysiologic mechanism linking elevated BMI and mood disorders and deserve further study as potential mood-regulating molecules.

Leptin predicts short-term major adverse cardiac events in patients with coronary artery disease

Introduction: Leptin is an adipose tissue-derived hormone associated with cardiovascular risk factors. We examined whether leptin predicts major adverse cardiac events (MACE) in coronary artery disease (CAD) patients.Methods: Fasting plasma leptin levels were measured in 1327 male and 619 female CAD patients. The patients were followed up for two years. The primary endpoint (MACE) was the composite of a hospitalisation for congestive heart failure (CHF) or a cardiac death. The secondary endpoint was the composite of an acute coronary syndrome (ACS) or a stroke.Results: In regression analysis including established risk variables, high leptin levels were associated with a significantly increased risk of MACE (HR 3.37; 95%CI 1.64–6.90; p = 0.001) and ACS or stroke (HR 1.95; 95%CI 1.29–2.96; p = 0.002). Adding leptin to the risk model for MACE increased the C-index from 0.78 (95%CI 0.71–0.85) to 0.81 (0.74–0.88) and improved classification (NRI 0.36; 95%CI 0.13–0.60; p = 0.002) and discrimination of the patients (IDI 0.016; 95%CI 0.001–0.030; p = 0.031).Conclusions: High plasma leptin levels predict short-term occurrence of CHF or cardiac death and ACS or stroke in patients with CAD independently of established risk factors. The possible harmful effects of leptin should be thoroughly investigated.Key messagesLeptin is a peptide hormone secreted mainly by adipose tissue. It has been associated with several cardiovascular risk factors.High leptin levels predict the short-term occurrence of congestive heart failure or cardiac death and ACS or stroke in patients with CAD independently of established risk factors.The possible detrimental effects of leptin on the cardiovascular system should be thoroughly investigated.

Obesity-related glomerulopathy: Mechanisms of development, clinical course

Obesity and overweight are recognized as epidemics of non-communicable diseases in the 21st century. The kidneys are a target organ for obesity, damage to which is considered to be an independent risk factor for the development of renal failure. Obesity-related glomerulopathy (OGP) is one of the types of renal injury in obesity, which is characterized by the development of proteinuria in patients with a body mass index (BMI) of >30 kg/m2 in the absence of other causes of kidney damage. The pathogenesis of OGP is multifactorial. It is associated with intrarenal hemodynamic disorders - the development of renal hyperfiltration, the damaging action of adipose tissue hormones (hyperleptinemia, activation of the renin-angiotensin-aldosterone system, decreased production of adiponectin); with ectopic lipid accumulation in the kidney. The morphological pattern of OGP is characterized by a low glomerular density (oligonephronia) that leads to glomerular and tubular hypertrophy; by the development of perihilar focal segmental glomerulosclerosis (FSGS), obvious podocyte damages, and the development of a fatty kidney. The clinical picture of OGP is characterized by the slow and gradual development of albuminuria, not exceeding Stage A3 (300-1999 mg/day). Approximately one-third of patients develop partial nephrotic syndrome with massive proteinuria, but without edema and hypoproteinemia. Complete nephrotic syndrome is observed in not more than 6% of patients with OGP. In the course of the disease, 50% of patients develop hypertension and more than 80% do dyslipidemia. Stages IV-V chronic kidney disease may develop 20-30 years after the disease occurs.

The long road to leptin

Leptin is an adipose tissue hormone that functions as an afferent signal in a negative feedback loop that maintains homeostatic control of adipose tissue mass. This endocrine system thus serves a critical evolutionary function by protecting individuals from the risks associated with being too thin (starvation) or too obese (predation and temperature dysregulation). Mutations in leptin or its receptor cause massive obesity in mice and humans, and leptin can effectively treat obesity in leptin-deficient patients. Leptin acts on neurons in the hypothalamus and elsewhere to elicit its effects, and mutations that affect the function of this neural circuit cause Mendelian forms of obesity. Leptin levels fall during starvation and elicit adaptive responses in many other physiologic systems, the net effect of which is to reduce energy expenditure. These effects include cessation of menstruation, insulin resistance, alterations of immune function, and neuroendocrine dysfunction, among others. Some or all of these effects are also seen in patients with constitutively low leptin levels, such as occur in lipodystrophy. Leptin is an approved treatment for generalized lipodystrophy, a condition associated with severe metabolic disease, and has also shown potential for the treatment of other types of diabetes. In addition, leptin restores reproductive capacity and increases bone mineral density in patients with hypothalamic amenorrhea, an infertility syndrome in females. Most obese patients have high endogenous levels of leptin, in some instances as a result of mutations in the neural circuit on which leptin acts, though in most cases, the pathogenesis of leptin resistance is not known. Obese patients with leptin resistance show a variable response to exogenous leptin but may respond to a combination of leptin plus amylin. Overall, the identification of leptin has provided a framework for studying the pathogenesis of obesity in the general population, clarified the nature of the biologic response to starvation, and helped to advance our understanding of the neural mechanisms that control feeding.

375 - Antioxidant Effect of Leptin on Neurogenic Niches in a Model of Alzheimer's Disease

Oxidative stress is implicated in the pathophysiology of a wide variety of neurodegenerative disorders and its role in neurogenesis is becoming increasingly acknowledged. It is known that the production of reactive oxygen species (ROS) is related to Alzheimer's disease (AD) progression and to the formation of Aβ plaques and tau neurofibrillary tangles. It has been show that leptin, an adipose tissue-derived hormone, is capable of reducing the amount of extracellular amyloid beta, tau phosphorylation in neuronal cells and can modulate neurogenesis in the adult hippocampus, although the mechanisms involved in this process in the AD brain are still unknown. Importantly, chronic administration of leptin resulted in a significant improvement in the cognitive performance of transgenic animal models. It is speculated that a deficiency in leptin levels or function may contribute to systemic and CNS abnormalities leading to disease progression. Here, we sought to determine if leptin is able to decreases the superoxide production in subventricular zone and hippocampus of double transgenic APP/PS1 and wild type mice. After 7 days of intraperitoneal administration of leptin, we estimated the oxidative stress levels. There was a significant decrease in superoxide production in the subgranular zone of the dentate gyrus and in the subventricular zone, as shown by DHE staining. We also observed an increasement of neurogenesis in these areas by immunostaining analysis. Our results indicate that acute administration of leptin decrease oxidative stress and increase cell proliferation in two neurogenic niches in the brain of Alzheimer’s Diseases model. We propose that targeting oxidative stress provides a novel way to regulate adult neurogenesis and manage different brain diseases such as AD.

Sex Hormone - Binding Globulin in Obese Type 2 Diabetics

Background: Obesity is one of risk factors for type 2 diabetes because of its association with insulin resistance and poor glycemic control. Sex hormone–binding globulin (SHBG) and adipose tissue hormones have a role in development of insulin resistance, hyperlipidemia and type 2 diabetes. Serum SHBG has a role in glucose homeostasis and low levels are associated with development of diabetes, cardiovascular diseases, insulin resistance and hyperinsulinemia. Aim of work: to study the relationship between serum SHBG, obesity, and metabolic parameters in type 2 diabetes in both sex. Patients and Methods: forty obese type 2 diabetic patients and ten obese non-diabetic as controls were included in this study. Blood was taking from all subjects for estimation of glucose, Lipid profile, insulin and SHBG. Results: there was highly significant decrease in mean serum SHBG concentration in diabetic group compared with control non diabetic group. There were significant negative associations between serum SHBG and age, disease duration, BMI and glucose. On the other hand, there were non significant correlations between SHBG and waist circumference, fasting insulin, HOMA-IR, cholesterol and triglyceride levels. Conclusion: Low serum SHBG is associated with hyperglycemia in both sexes, independent of insulinemia

Olanzapine-depot administration induces time-dependent changes in adipose tissue endocrine function in rats

ObjectiveMetabolic adverse effects of atypical antipsychotics (AAP) contribute significantly to increased risk of cardiovascular morbidity and mortality in patients suffering from schizophrenia. Extensive preclinical research has addressed this issue over the past years, though mechanisms underlying these adverse effects of AAP are still not understood completely. Recently, attention is drawn towards the role of adipose tissue metabolism and neurohormonal regulations. MethodsThe aim of this study was to evaluate the time-dependent effects of olanzapine depot administration at clinically relevant dosing on the regulation of energy homeostasis, glucose and lipid metabolism, gastrointestinal and adipose tissue-derived hormones involved in energy balance regulations in female Sprague-Dawley rats. The study lasted 8 weeks and the markers were assayed at day 8, 15, 29, 43 and 57. ResultsThe results indicate that in the absence of hyperphagia, olanzapine chronic exposure induced weight gain from the beginning of the study. In the later time-point, increased adiposity was also observed. In the initial phase of the study, lipid profile was altered by an early increase in triglyceride level and highly elevated leptin level was observed. Clear bi-phasic time-dependent effect of olanzapine on leptin serum concentration was demonstrated. Olanzapine treatment did not lead to changes in serum levels of ghrelin, FGF-21 and pro-inflammatory markers IL-1a, IL-6 and TNF-α at any time-point of the study. ConclusionThis study provides data suggesting early alteration in adipose tissue endocrine function as a factor involved in mechanisms underlying metabolic adverse effects of antipsychotics.

Effect of islamic fasting on glucose, lipid profiles and Body Mass Index, adiponectin and leptin in obese individuals

Introduction: Fasting is an Islamic practice, which causes various metabolic changes in fasting individuals. Numerous studies have examined different aspects of fasting, but its effect on individuals with different characteristics such as obesity has remained unknown. The impact of fasting on adipose tissue hormones such as leptin and adiponectin is still controversial. In this study, we aimed to examine the effect of Islamic fasting on glucose and lipid profiles, as well as plasma adiponectin and leptin concentrations in fasting obese and normal-weight individuals. Methods: Obese and normal-weight individuals from Yazd, Iran, who fasted during Ramadan were divided into two groups (n=24). Blood samples were taken from all the participants after 10-12 fasting hours two days before and one day after Ramadan to assess glucose and lipid profiles and plasma adiponectin and leptin concentrations. The individuals who were not able to fast for at least 21 days due to inflammatory or infectious diseases and those who received oral medications or supplements during Ramadan were excluded from the study. Results: Variations in weight, body mass index (BMI), total cholesterol, high-density lipoprotein cholesterol (HDL-c), the ratio of total cholesterol to HDL-c were significant in the obese group (P<0.05). There were no significant changes in leptin and adiponectin levels in obese cases. Variables such as weight, BMI, and triglycerides and leptin levels decreased significantly, while adiponectin level did not change significantly in normal-weight cases. Conclusion: Islamic fasting can prevent cardiovascular diseases in obese and normal-weight individuals through reducing weight, BMI, and some blood lipids, elevating HDL-c level, and changing the concentration of some adipokines.

Circulating betatrophin in healthy control and type 2 diabetic subjects and its association with metabolic parameters

AimsBetatrophin, a newly identified liver and adipose tissue-derived hormone, has been suggested as an inducer of β-cell proliferation in mice. However, the physiological role of betatrophin remains poorly understood in humans. Hence, the aim of this study was to investigate circulating betatrophin concentrations in normal and type 2 diabetes mellitus (T2DM) Saudi subjects and its association with various metabolic parameters. MethodsIn this cross-sectional study, 200 Saudi adults (81 healthy non-T2DM controls, age: 41.43±8.35 [mean±SD]; BMI: 31.58±5.49 and 119 T2DM subjects, age: 48.78±11.76years; BMI: 30.25±4.83kg/m2) were studied. Anthropometric and fasting serum biochemical data were collected. Circulating betatrophin was measured using an enzyme-linked immunosorbent assay (ELISA) based kit. ResultsWe observed significantly higher levels of betatrophin in T2DM subjects compared to healthy controls (882.19±329.06 vs 657.14±261.04pg/ml, p<0.001). Furthermore, in T2DM subjects, betatrophin level was positively associated with blood pressure and serum fasting glucose (p<0.05). ConclusionsOur results suggest that circulating betatrophin is significantly elevated in subjects with T2DM compared to healthy controls. Increase in the level of betatrophin in T2DM subjects might be a compensatory mechanism for enhanced insulin demand in T2DM condition.