Normalizing adiponectin levels in obese pregnant mice prevents adverse metabolic outcomes in offspring

Paulsen, Megan E.; Rosario, Fredrick J.; Wesolowski, Stephanie R.; Powell, Theresa L.; Jansson, Thomas

doi:10.1096/fj.201801015r

Cited by 33 publications

(33 citation statements)

References 55 publications

(81 reference statements)

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“…Maternal adiponectin infusion in these obese mice led to a normalisation of maternal insulin sensitivity, nutrient transport, placental insulin/mTORC1 and PPARα signalling and fetal growth independent of the effects on maternal fat mass (Aye et al 2015). Further work by Paulsen et al has also shown that normalisation of adiponectin levels of maternal obesity in the mouse prevented the development of adverse metabolic outcomes in male offspring (Paulsen et al 2018) and thus suggests that low circulating maternal adiponectin may represent a critical mechanistic link between a maternal obesogenic environment and the development of metabolic disease in offspring.…”

Section: Intervention Strategiesmentioning

confidence: 92%

The role of adipokines in developmental programming: evidence from animal models

Reynolds

Vickers

2019

Journal of Endocrinology

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Alterations in the environment during critical periods of development, including altered maternal nutrition, can increase the risk for the development of a range of metabolic, cardiovascular and reproductive disorders in offspring in adult life. Following the original epidemiological observations of David Barker that linked perturbed fetal growth to adult disease, a wide range of experimental animal models have provided empirical support for the developmental programming hypothesis. Although the mechanisms remain poorly defined, adipose tissue has been highlighted as playing a key role in the development of many disorders that manifest in later life. In particular, adipokines, including leptin and adiponectin, primarily secreted by adipose tissue, have now been shown to be important mediators of processes underpinning several phenotypic features associated with developmental programming including obesity, insulin sensitivity and reproductive disorders. Moreover, manipulation of adipokines in early life has provided for potential strategies to ameliorate or reverse the adverse sequalae that are associated with aberrant programming and provided insight into some of the mechanisms involved in the development of chronic disease across the lifecourse.

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Section: Intervention Strategiesmentioning

confidence: 92%

The role of adipokines in developmental programming: evidence from animal models

Reynolds

Vickers

2019

Journal of Endocrinology

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“…In the grouped analyses, male offspring of dams on control diet were used as the control group. Experimental numbers (n/group) were determined using previous studies by our group [ 43 ], as well as expertise from the mouse phenotyping core at The University of Minnesota. Data are presented as mean ± SEM.…”

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

“…In this mouse model of HFHC-induced maternal obesity, we previously observed that male, but not female, HFHC offspring, gain excess weight at 8–9 weeks postnatal age on a standard chow diet [ 43 ]. At 14 weeks of age, maternal HFHC-diet-exposed male offspring, but not female offspring, show evidence of adiposity, glucose intolerance, insulin resistance, fatty liver, and cardiac dysfunction [ 43 , 44 ]. Neither a hypothalamic phenotype or evaluation of potential programming mechanisms at earlier timepoints in offspring, i.e., prior to the onset of weight gain and metabolic dysfunction, were evaluated in this maternal HFHC-induced obesity animal model [ 27 , 43 , 44 , 45 , 46 , 47 ].…”

Section: Introductionmentioning

confidence: 99%

“…The objective of our study was to investigate hypothalamus-mediated energy homeostasis in offspring, following exposure to maternal HFHC diet and obesity, at a developmental time-point prior to previously observed weight gain and metabolic disease [ 43 ] We chose to study peripubertal offspring (28–40-days old), as this time point was developmentally equivalent to the hypothalamic development of term infants [ 3 , 28 ]. Additionally, we studied males and females separately.…”

Section: Introductionmentioning

confidence: 99%

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Maternal High-Fat–High-Carbohydrate Diet-Induced Obesity Is Associated with Increased Appetite in Peripubertal Male but Not Female C57Bl/6J Mice

Kulhanek¹,

Weigel²,

Paulsen³

2020

Nutrients

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Diet-induced maternal obesity might play a critical role in altering hypothalamic development, predisposing the offspring to obesity and metabolic disease later in life. The objective of this study was to describe both phenotypic and molecular sex differences in peripubertal offspring energy homeostasis, using a mouse model of maternal obesity induced by a high-fat–high-carbohydrate (HFHC) diet. We report that males, not females, exposed to a maternal HFHC diet had increased energy intake. Males exposed to a maternal HFHC diet had a 15% increased meal size and a 46% increased frequency, compared to the control (CON) males, without a change in energy expenditure. CON and HFHC offspring did not differ in body weight, composition, or plasma metabolic profile. HFHC diet caused decreased hypothalamic glucocorticoid expression, which was further decreased in males compared to females. Maternal weight, maternal caloric intake, and male offspring meal frequency were inversely correlated with offspring hypothalamic insulin receptor (IR) expression. There was a significant interaction between maternal-diet exposure and sex in hypothalamic IR. Based on our preclinical data, we suggest that interventions focusing on normalizing maternal nutrition might be considered to attenuate nutritional influences on obesity programming and curb the continuing rise in obesity rates.

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Rapid responses of adipocytes to iron overload increase serum TG level by decreasing adiponectin

Tang

Wang

Zhang

et al. 2021

Journal Cellular Physiology

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Iron overload is tightly connected with metabolic disorders. Excess iron in the adipose and its roles in dyslipidemia are of interest to be identified. In acute iron overload mice receiving intraperitoneal injection of 100 mg/kg/day dextran-iron for 5 days, the epididymis adipose showed a remarkable increase in iron. Serum triglyceride and low-density lipoprotein cholesterol (LDL-C) levels were increased and high-density lipoprotein cholesterol (HDL-C) level was decreased, while serum alkaline phosphatase, aspartate aminotransferase, glucose, and insulin were not affected. The serum-cytokine-microarray showed that adipocytokines, including adiponectin, leptin, and resistin were significantly decreased. Other serum cytokines, including pro-insulin cytokines, inflammatory cytokines, chemokines, and growth factors were not changed, except that ghrelin and chemokine RANTES were increased. Iron overload decreased expressions of adiponectin and leptin both in vivo and in vitro. Intraperitoneal injection of recombinant leptin at 1 μg/g in acute iron overload mice had no significant effects on serum levels of TC, TG, HDL-C, and LDL-C, while intraperitoneal injection of recombinant adiponectin at 3 μg/g partially restored serum TG level through improving activities of lipoprotein lipase and hepatic lipase, but abnormal serum LDL-C and HDL-C were not redressed, suggesting other mechanisms also existed. In conclusion, the adipose responds to iron overload at an early stage to interfere with lipid metabolism by secreting adipocytokines, which may further affect glucose metabolism, inflammation, and other iron overload-induced effects on the body.

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Normalizing adiponectin levels in obese pregnant mice prevents adverse metabolic outcomes in offspring

Cited by 33 publications

References 55 publications

The role of adipokines in developmental programming: evidence from animal models

The role of adipokines in developmental programming: evidence from animal models

Maternal High-Fat–High-Carbohydrate Diet-Induced Obesity Is Associated with Increased Appetite in Peripubertal Male but Not Female C57Bl/6J Mice

Rapid responses of adipocytes to iron overload increase serum TG level by decreasing adiponectin

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