The aim of the present study was to investigate the relationship between leptin and adiponectin gene polymorphisms, circulating levels of leptin and adiponectin, adiposity and clinical markers in patients with myelodysplastic syndrome (MDS). This cross-sectional study was conducted with 102 adults and elderly MDS patients and 102 age- and sex-matched controls. Clinical characteristics, co-morbidities, anthropometric data, laboratory evaluation and genetic analysis (polymorphisms −2548G > A/rs7799039 of the LEP gene and +276G > T/rs1501299 of the ADIPOQ gene) were investigated. Serum leptin was higher and adiponectin lower in MDS when compared with controls. There was a significant positive correlation between serum leptin levels and BMI (r = 0·264, P = 0·025), waist circumference (r = 0·235, P = 0·047), body fat percentage (BF %) (r = 0·373, P = 0·001) and the fat mass index (FMI) (r = 0·371, P < 0·001). A lower mean adiponectin was found among patients with high BF %, higher visceral adiposity index and metabolic syndrome. A significant association was found between the AA genotype (mutant) of the LEP polymorphism rs7799039 and male sex and blast excess (≥ 5 %). In addition, a significant association was observed between the TT genotype (mutant) of the ADIPOQ rs1501299 polymorphism and Fe overload. These results demonstrate the importance of a comprehensive and systematic evaluation in patients with MDS in order to identify and control negative factors not related to the disease at an early stage.

Maternal diet during pregnancy has been associated with obesity among offspring. The extent to which trimester-specific dietary patterns are associated with markers of adiposity during adolescence remains unclear. We examined associations between prenatal diet patterns with adolescent offspring measures of adiposity and adipokines in 384 mother–adolescent dyads from the Mexico City ELEMENT cohort. Trimester-specific diet patterns were derived from principal component analysis of food frequency questionnaire data. Adolescent anthropometry and serum leptin and adiponectin were measured at 10–17 years. Three maternal diet patterns were identified: Prudent Diet (PD), high in fish and vegetables, the High Meat and Fat Diet (HMFD), high in pork and processed meats, and the Transitioning Mexican Diet (TMD), high in corn tortillas and sugar-sweetened beverages. Multiple linear regression was used to estimate sex-stratified associations among quartiles of diet patterns with adiposity and adipokines, adjusting for maternal marital status, education, and parity. First trimester TMD was associated with greater anthropometric measures and higher leptin in females, while third trimester HMFD was associated higher body fat percentage, triceps thickness, waist circumference, and leptin, but lower adiponectin among males. Contrary to expectation, there were positive associations between the trimester 1 PD pattern and anthropometric measurements in females, and for trimester 2 HMFD and TMD patterns with adipokines among males. Findings suggest maternal diet patterns may influence offspring adiposity markers during adolescence in a sex-specific manner.

Health in pregnancy and infancy can affect the risk of chronic non-communicable diseases. We aimed to describe leptin and adiponectin concentrations in low birth weight (LBW) infants and identify possible associations with maternal nutritional status, adequacy for gestational age, nutritional recovery, and current dietary intake. A cross-sectional study with LBW infants (9–12 months) including maternal background and pre-pregnancy nutritional condition was performed. From the Infants: anthropometry at birth and current was expressed as z-score (weight: WAZ, length, head circumference), nutritional recovery, dietary intake, leptin, and adiponectin blood concentrations. The mean age of the 54 infants was 10.0 ± 1.5 months, 32 (59.3%) were female, 36 (66.7%) preterm, 23 (42.6%) small for gestational age (SGA), and 25 pregnancies (46.3%) were twin. Almost all (98%) of the infants intake energy and protein above the recommendation, and 47 (87.6%) consumed ultra-processed foods. At the time of the assessment, 8 (14.8%) were overweight and 4 (7.4%) had short stature. SGA infants showed faster weight recovery (WAZ 1.54; 95% CI 1.17, 1.91; p = 0.001), higher leptin’s concentration (3.0 ng/ml (1.7, 3.0) versus 1.6 ng/ml (0.9, 2.6); p = 0.032)), and leptin/adiponectin ratio (0.13 ± 0.08 versus 0.07 ± 0.07; p = 0.018). The pre-gestational BMI was a modifier of the effect of WAZ on leptin levels (p = 0.027) in LBW infants. Higher pre-gestational BMI increased the effect of WAZ variation (birth and current) on leptin levels. Concluding, LBW infants showed early changes in leptin and adiponectin concentrations, influenced by maternal (pre-gestational BMI), intrauterine (gestational age adequacy – SGA), and postnatal weight gain. This combination of factors may increase the risk of NCD for this group of children.

The paper is based on the lecture that I gave on receiving the Nutrition Society's inaugural Gowland Hopkins Award for contributions to Cellular and Molecular Nutrition. It reviews studies on the adipose tissues, brown and white, conducted by the groups that I have led since entering nutrition research in 1975. The initial focus was on exploring metabolic factors that underpin the development of obesity using animal models. This resulted in an interest in non-shivering thermogenesis with brown adipose tissue being identified as the key effector of facultative heat production. Brown fat is less thermogenically active in various obese rodents, and major changes in activity are exhibited under physiological conditions such as lactation and fasting consistent with a general role for the tissue in nutritional energetics. My interests moved to white adipose tissue following the cloning of the Ob gene. Our initial contributions in this area included demonstrating nutritional regulation of Ob gene expression and circulating leptin levels, as well as a regulatory role for the sympathetic nervous system operating through β3-adrenoceptors. My interests subsequently evolved to a wider concern with the endocrine/signalling role of adipose tissue. Inflammation is a characteristic of white fat in obesity with the release of inflammation-related adipokines, and we proposed that hypoxia underlies this inflammatory state. O2-deprivation was shown to have substantial effects on gene expression and cellular function in white adipocytes. The hypoxia studies led to the proposition that O2 should be considered as a critical macronutrient.

Fetal programming by androgen excess is hypothesized as one of the main factors contributing to the development of polycystic ovary syndrome (PCOS). PCOS is more than a reproductive disorder, as women with PCOS also show metabolic and other endocrine alterations. Since both ovarian and reproductive functions depend on energy balance, the alterations in metabolism may be related to reproductive alterations. The present study aimed to evaluate the effect of androgen excess during prenatal life on ovarian fuel sensors and its consequences on steroidogenesis. To this end, pregnant rats were hyperandrogenized with testosterone and the following parameters were evaluated in their female offspring: follicular development, PPARG levels, adipokines (including leptin, adiponectin, and chemerin as ovarian fuel sensors), serum gonadotropins (LH and FSH), the mRNA of their ovarian receptors, and the expression of steroidogenic mediators. At 60 days of age, the prenatally hyperandrogenized (PH) female offspring displayed both an irregular ovulatory phenotype and an anovulatory phenotype with altered follicular development and the presence of cysts. Both PH groups showed altered levels of both proteins and mRNA of PPARG and a different expression pattern of the adipokines studied. Although serum gonadotropins were not impaired, there were alterations in the mRNA levels of their ovarian receptors. The steroidogenic mediators Star, Cyp11a1, Cyp17a1, and Cyp19a1 were altered differently in each of the PH groups. We concluded that androgen excess during prenatal life leads to developmental programming effects that affect ovarian fuel sensors and steroidogenesis in a phenotype-specific way.

This study aimed to evaluate the longitudinal association of vitamin D status with glycaemia, insulin, homoeostatic model assessment of insulin resistance, adiponectin and leptin. A prospective cohort with 181 healthy, pregnant Brazilian women was followed at the 5th–13th, 20th–26th and 30th–36th gestational weeks. In this cohort, 25-hydroxyvitamin D (25(OH)D) plasma concentrations were analysed using liquid chromatography–tandem MS. Vitamin D status was categorised as sufficient or insufficient using the Endocrine Society Practice Guidelines (≥75/<75 nmol/l) and the Institute of Medicine (≥50/<50 nmol/l) thresholds. Linear mixed-effect regression models were employed to evaluate the association between vitamin D status and each outcome, considering interaction terms between vitamin D status and gestational age (P<0·1). At baseline, 70·7 % of pregnant women had 25(OH)D levels <75 nmol/l and 16 % had levels <50 nmol/l. Women with sufficient vitamin D status at baseline, using both thresholds, presented lower glycaemia than those with insufficient 25(OH)D. Pregnant women with 25(OH)D concentrations <75 nmol/l showed lower insulin (β=−0·12; 95 % CI −0·251, 0·009; P=0·069) and adiponectin (β=−0·070; 95 % CI −0·150, 0·010; P=0·085) concentrations throughout pregnancy than those with 25(OH)D levels ≥75 nmol/l. Pregnant women with 25(OH)D <50 nmol/l at baseline presented significantly higher leptin concentrations than those with 25(OH)D levels ≥50 nmol/l (β=−0·253; 95 % CI −0·044, 0·550; P=0·095). The baseline status of vitamin D influences the biomarkers involved in glucose metabolism. Vitamin D-sufficient women at baseline had higher increases in insulin and adiponectin changes throughout gestation than those who were insufficient.

Diet, obesity and adipokines play important roles in diabetes and CVD; yet, limited studies have assessed the relationship between diet and multiple adipokines. This cross-sectional study assessed associations between diet, adiposity and adipokines in Mexican Americans. The cohort included 1128 participants (age 34·7±8·2 years, BMI 29·5±5·9 kg/m2, 73·2 % female). Dietary intake was assessed by 12-month food frequency questionnaire. Adiposity was measured by BMI, total percentage body fat and percentage trunk fat using dual-energy X-ray absorptiometry. Adiponectin, apelin, C-reactive protein (CRP), dipeptidyl peptidase-4 (DPP-IV), IL-1β, IL-1ra, IL-6, IL-18, leptin, lipocalin, monocyte chemo-attractant protein-1 (MCP-1), resistin, secreted frizzled protein 4 (SFRP-4), SFRP-5, TNF-α and visfatin were assayed with multiplex kits or ELISA. Joint multivariate associations between diet, adiposity and adipokines were analysed using canonical correlations adjusted for age, sex, energy intake and kinship. The median (interquartile range) energy intake was 9514 (7314, 11912) kJ/d. Overall, 55 % of total intake was accounted for by carbohydrates (24 % from sugar). A total of 66 % of the shared variation between diet and adiposity, and 34 % of diet and adipokines were explained by the top canonical correlation. The diet component was most represented by sugar-sweetened beverages (SSB), fruit and vegetables. Participants consuming a diet high in SSB and low in fruits and vegetables had higher adiposity, CRP, leptin, and MCP-1, but lower SFRP-5 than participants with high fruit and vegetable and low SSB intake. In Mexican Americans, diets high in SSB but low in fruits and vegetables contribute to adiposity and a pro-inflammatory adipokine profile.

Some studies have shown that expression of peroxisome proliferator-activated receptor gamma (PPARG), a key regulator of adipogenesis, and of some adipocyte-specific genes or adipokines are expressed in hepatic steatosis, leading to the concept of ‘adipogenic hepatic steatosis’ or ‘hepatic adiposis.’ Most of these studies were conducted in genetic obese mouse models or after manipulation of gene expression. The relevance of this concept to other species and more physiological models was here addressed in ducks which are able to develop hepatic steatosis after overfeeding. The expression of PPARG and other adipocyte-specific genes was thus analyzed in the liver of ducks fed ad libitum or overfed and compared with those observed in adipose tissues. Pekin (Anas platyrhynchos) and Muscovy ducks (Cairina moschata) were analyzed, as metabolic responses to overfeeding differ according to these two species, Muscovy ducks having a greater ability to synthesize and store lipids in the liver than Pekin ducks. Our results indicate that adipocyte-specific genes are expressed in the liver of ducks, PPARG and fatty acid-binding protein 4 being upregulated and adiponectin and leptin receptor downregulated by overfeeding. However, these expression levels are much lower than those observed in adipose tissue suggesting that fatty liver cells are not transformed to adipocytes, although some hepato-specific functions are decreased in fatty liver when compared with normal liver.

At birth, when immune responses are insufficient, there begins the development of the defence capability against pathogens. Leptin and adiponectin, adipokines that are present in breast milk, have been shown to play a role in the regulation of immune responses. We report here, for the first time, the influence of in vivo adipokine supplementation on the intestinal immune system in early life. Suckling Wistar rats were daily supplemented with leptin (0·7 μg/kg per d, n 36) or adiponectin (35 μg/kg per d, n 36) during the suckling period. The lymphocyte composition, proliferation and cytokine secretion from mesenteric lymph node lymphocytes (on days 14 and 21), as well as intestinal IgA and IgM concentration (day 21), were evaluated. At day 14, leptin supplementation significantly increased the TCRαβ+ cell proportion in mesenteric lymph nodes, in particular owing to an increase in the TCRαβ+ CD8+ cell population. Moreover, the leptin or adiponectin supplementation promoted the early development CD8+ cells, with adiponectin being the only adipokine capable of enhancing the lymphoproliferative ability at the end of the suckling period. Although leptin decreased intestinal IgA concentration, it had a trophic effect on the intestine in early life. Supplementation of both adipokines modulated the cytokine profile during (day 14) and at the end (day 21) of the suckling period. These results suggest that leptin and adiponectin during suckling play a role in the development of mucosal immunity in early life.

The aim of this study was to evaluate the association of dietary patterns (DP) with maternal adiposity indicators, leptin, adiponectin and insulin concentrations during pregnancy. A prospective cohort of pregnant women followed up at the 5th–13th, 20th –26th and 30th–36th gestational weeks and 30–40 d postpartum was conducted in Rio de Janeiro. A FFQ was administered in the third trimester (30th–36th gestational weeks). The reduced rank regression procedure was used to identify DP that explain response variables (dietary fibre and total fat) related to indicators of maternal adiposity (postpartum weight retention and gestational weight gain (GWG) adequacy), and plasma leptin, adiponectin and insulin concentrations. The associations between tertiles of DP and the outcomes were determined using logistic regression or longitudinal linear mixed-effect regression models. The mean daily energy intake during pregnancy was 10 104 (sd 3234) kJ (2415 (sd 773) kcal), and GWG was 11·9 (sd 4·2) kg. In all, 40 % of women presented pre-gestational overweight/obesity. Excessive GWG occurred in 34·7 % of pregnant women and 56·6 % were overweight/obese at postpartum. The ‘common-Brazilian’ DP (characterised by higher intake of beans, rice and lower intake of fast food/snacks, candies/table sugar and processed meats/bacon) was positively associated with adiponectin (β=1·07; 95 % CI 0·17, 1·98). The ‘Western’ DP (characterised by higher intake of fast food/snacks and processed meat/bacon and lower intake of noodles/pasta/roots/tubers and sodas) was negatively associated with adiponectin (β=−1·11; 95 % CI −2·00, −0·22) and positively associated with leptin concentrations (β=64·9; 95 % CI 22·8, 107·0) throughout pregnancy. It may be suggested that the ‘common-Brazilian’ is a healthy DP and beneficial for serum concentrations of adiponectin and leptin.

Dietary indices have been related to risk for type 2 diabetes (T2D) predominantly in white populations. The present study evaluated this association in the ethnically diverse Multiethnic Cohort and examined four diet quality indices in relation to T2D risk, homoeostatic model assessment-estimated insulin resistance (HOMA-IR) and biomarkers of dyslipidaemia, inflammation and adipokines. The T2D analysis included 166 550 white, African American, Native Hawaiian, Japanese American and Latino participants (9200 incident T2D cases). Dietary intake was assessed at baseline using a quantitative FFQ and T2D status was based on three self-reports and confirmed by administrative data. Biomarkers were assessed about 10 years later in a biomarker subcohort (n 10 060). Sex- and ethnicity-specific hazard ratios were calculated for the Healthy Eating Index-2010 (HEI-2010), the alternative HEI-2010 (AHEI-2010), the alternate Mediterranean diet score (aMED) and the Dietary Approaches to Stop Hypertension (DASH). Multivariable-adjusted means of biomarkers were compared across dietary index tertiles in the biomarker subcohort. The AHEI-2010, aMED (in men only) and DASH scores were related to a 10–20 % lower T2D risk, with the strongest associations in whites and the direction of the relationships mostly consistent across ethnic groups. Higher scores on the four indices were related to lower HOMA-IR, TAG and C-reactive protein concentrations, not related to leptin, and the DASH score was directly associated with adiponectin. The AHEI-2010 and DASH were directly related to HDL-cholesterol in women. Potential underlying biological mechanisms linking diet quality and T2D risk are an improved lipid profile and reduced systemic inflammation and, with regards to DASH alone, an improved adiponectin profile.

Gestational diabetes mellitus (GDM) is a serious problem growing worldwide that needs to be addressed with urgency in consideration of the resulting severe complications for both mother and fetus. Growing evidence indicates that a healthy diet rich in fruit, vegetables, nuts, extra-virgin olive oil and fish has beneficial effects in both the prevention and management of several human diseases and metabolic disorders. In this review, we discuss the latest data concerning the effects of dietary bioactive compounds such as polyphenols and PUFA on the molecular mechanisms regulating glucose homoeostasis. Several studies, mostly based on in vitro and animal models, indicate that dietary polyphenols, mainly flavonoids, positively modulate the insulin signalling pathway by attenuating hyperglycaemia and insulin resistance, reducing inflammatory adipokines, and modifying microRNA (miRNA) profiles. Very few data about the influence of dietary exposure on GDM outcomes are available, although this approach deserves careful consideration. Further investigation, which includes exploring the ‘omics’ world, is needed to better understand the complex interaction between dietary compounds and GDM.

Nutritional stressors may cause negative effects on animal health and growth and lead to significant economic impact. Adipose tissue is an endocrine organ producing, mediators and hormones, called adipokines. They play a dynamic role in body homeostasis and in the regulation of energy expenditure, interacting with feeding behavior, hormones and growth factors. This in vitro study aimed to investigate how nutritional conditions and growth hormone (GH) can influence nitric oxide (NO) production and the expression and secretion of three important adipokines, that is leptin, interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α), by swine adipocytes. In our experimental model, mesenchymal stem cells from omental adipose tissue were induced to adipogenic differentiation. After differentiation, adipocytes were incubated for 24 h (T0) with DMEM/Ham’s F12 (group A) or DMEM/Ham’s F12 salts (group B), a DMEM/Ham’s F12 formulation deprived of nutritional components. Primary adipocyte cells were also co-cultured for 4 h (T+4) or 12 h (T+12) with or without anterior pituitary slices. To stimulate GH secretion by pituitary cells, growth hormone releasing hormone at 10−8 M was added at the start of the incubation times (4 or 12 h). At T0, T+4 and T+12, NO production, leptin, IL-6 and TNF-α expression and secretion were measured. NO increased (P<0.05) up to twofold in restricted culture conditions. Deprived medium and coincubation with anterior pituitary positively influenced leptin secretion and expression. TNF-α was expressed and secreted only in deprived culture condition groups (B, B1 and B2). Nutrients availability and pituitary co-culture did not affect IL-6 expression and secretion. Our study shows an endocrine function for porcine adipocytes. In our model, adipocytes readily responded to nutritional inputs by secretion of molecules affecting energy balance. This secretion capacity was modulated by GH. Improving our knowledge of the role of adipocyte in the endocrine system, may lead to a more complete understanding of regulating energy balance in swine.

The mechanism behind the beneficial effects of enteral nutrition (EN) for patients with acute pancreatitis (AP) is largely unknown. Adipokines, as mediators of metabolism and inflammation, may be a possible mechanism. The study aimed to investigate the effect of EN on adipokines early in the course of AP. Patients with AP were randomised to EN or nil-by-mouth (NBM). Blood samples were taken on the first 4 d of admission and adipokine concentrations for adiponectin, leptin, omentin, resistin and visfatin were determined by ELISA assays. A linear mixed model analysis was run to determine differences in adipokine concentrations between the two study groups. A total of thirty-two patients were included in the study. Omentin concentrations were significantly higher in patients who received EN compared with NBM across the first 4 d of admission (mean difference: 11·6 (95 % CI 1·0, 22·3) ng/ml; P = 0·033). Leptin concentrations were significantly higher in patients who received EN compared with NBM after adjusting for age, sex and BMI (mean difference: 2·3 (95 % CI 0·1, 4·5) ng/ml; P = 0·037). No significant difference in adiponectin, resistin or visfatin concentrations were observed between the two study groups. EN significantly increases omentin and leptin concentrations in AP. Future research should be directed towards understanding whether these adipokines are responsible for the therapeutic benefits of EN.

Observational studies have suggested that 25-hydroxyvitamin D (25(OH)D) levels are associated with inflammatory markers. Most trials reporting significant associations between vitamin D intake and inflammatory markers used specific patient groups. Thus, we aimed to determine the effect of supplementary vitamin D using secondary data from a population-based, randomised, placebo-controlled, double-blind trial (Pilot D-Health trial 2010/0423). Participants were 60- to 84-year-old residents of one of the four eastern states of Australia. They were randomly selected from the electoral roll and were randomised to one of three trial arms: placebo (n 214), 750 μg (n 215) or 1500 μg (n 215) vitamin D3, each taken once per month for 12 months. Post-intervention blood samples for the analysis of C-reactive protein (CRP), IL-6, IL-10, leptin and adiponectin levels were available for 613 participants. Associations between intervention group and biomarker levels were evaluated using quantile regression. There were no statistically significant differences in distributions of CRP, leptin, adiponectin, leptin:adiponectin ratio or IL-10 levels between the placebo group and either supplemented group. The 75th percentile IL-6 level was 2·8 pg/ml higher (95 % CI 0·4, 5·8 pg/ml) in the 1500 μg group than in the placebo group (75th percentiles:11·0 v. 8·2 pg/ml), with a somewhat smaller, non-significant difference in 75th percentiles between the 750 μg and placebo groups. Despite large differences in serum 25(OH)D levels between the three groups after 12 months of supplementation, we found little evidence of an effect of vitamin D supplementation on cytokine or adipokine levels, with the possible exception of IL-6.

Undernutrition in early life has been reported to be closely associated with the development of non-communicable diseases in adulthood. Adequate treatment is important for reversing these effects. In the present study, we investigated the effects of undernutrition and anthropometric recovery on the weights and heights of children in relation to the concentrations of leptin, adiponectin and plasminogen activator inhibitor-1 (PAI-1). A total of 119 children (aged 6–16 years) from the slums of São Paulo were selected according to their nutritional status and divided into three groups as follows: control (healthy without intervention, n 38) with a height-for-age Z score (HAZ) and a BMI-for-age Z score (BAZ) > − 1·6; undernourished (HAZ and/or BAZ < − 1·6, n 54); recovered from undernutrition (after treatment in a rehabilitation centre; HAZ and BAZ > − 1·6, n 27). Blood samples were collected to determine insulin, glucose, leptin, adiponectin and PAI-1 concentrations. Leptin concentrations in the undernourished group were lower than those in the control and recovered groups (mean 0·92 (95 % CI 0·67, 1·25), 2·03 (95 % CI 1·46, 2·82) and 1·66 (95 % CI 1·15, 2·44) ng/ml, P= 0·003), which had similar leptin concentrations. There were no differences in adiponectin and PAI-1 concentrations among the groups. A positive correlation between waist circumference and leptin concentrations was observed in all the girls and boys of the control group (control: r 0·729, P< 0·01; undernourished: r 0·490, P< 0·05; and recovered: r 0·829, P< 0·01; r 0·673, P< 0·05). Stronger correlations between leptin and insulin concentrations were observed in the recovered group. The results of the present study indicate that normal leptin concentrations are found when normal height and weight are achieved.

In adipocytes the hydrolysis of TAG to produce fatty acids and glycerol under fasting conditions or times of elevated energy demands is tightly regulated by neuroendocrine signals, resulting in the activation of lipolytic enzymes. Among the classic regulators of lipolysis, adrenergic stimulation and the insulin-mediated control of lipid mobilisation are the best known. Initially, hormone-sensitive lipase (HSL) was thought to be the rate-limiting enzyme of the first lipolytic step, while we now know that adipocyte TAG lipase is the key enzyme for lipolysis initiation. Pivotal, previously unsuspected components have also been identified at the protective interface of the lipid droplet surface and in the signalling pathways that control lipolysis. Perilipin, comparative gene identification-58 (CGI-58) and other proteins of the lipid droplet surface are currently known to be key regulators of the lipolytic machinery, protecting or exposing the TAG core of the droplet to lipases. The neuroendocrine control of lipolysis is prototypically exerted by catecholaminergic stimulation and insulin-induced suppression, both of which affect cyclic AMP levels and hence the protein kinase A-mediated phosphorylation of HSL and perilipin. Interestingly, in recent decades adipose tissue has been shown to secrete a large number of adipokines, which exert direct effects on lipolysis, while adipocytes reportedly express a wide range of receptors for signals involved in lipid mobilisation. Recently recognised mediators of lipolysis include some adipokines, structural membrane proteins, atrial natriuretic peptides, AMP-activated protein kinase and mitogen-activated protein kinase. Lipolysis needs to be reanalysed from the broader perspective of its specific physiological or pathological context since basal or stimulated lipolytic rates occur under diverse conditions and by different mechanisms.

According to human research, the location of fat accumulation seems to play an important role in the induction of obesity-related inflammatory complications. To evaluate whether an inflammatory response to obesity depends on adipose tissue location, adipokine gene expression, presence of immune cells and adipocyte cell size of subcutaneous adipose tissue (SAT) and visceral adipose tissue (VAT) were compared between lean and obese cats. Additionally, the present study proposes the cat as a model for human obesity and highlights the importance of animal models for human research. A total of ten chronically obese and ten lean control cats were included in the present study. Body weight, body condition score and body composition were determined. T-lymphocyte, B-lymphocyte, macrophage concentrations and adipocyte cell size were measured in adipose tissue at different locations. Serum leptin concentration and the mRNA expression of leptin and adiponectin, monocyte chemoattractant protein-1, chemoligand-5, IL-8, TNF-α, interferon-γ, IL-6 and IL-10 were measured in blood and adipose tissues (abdominal and inguinal SAT, and omental, bladder and renal VAT). Feline obesity was characterised by increased adipocyte cell size and altered adipokine gene expression, in favour of pro-inflammatory cytokines and chemokines. Consequently, concentration of T-lymphocytes was increased in the adipose tissue of obese cats. Alteration of adipose tissue was location dependent in both lean and obese cats. Moreover, the observed changes were more prominent in SAT compared with VAT.