Leptin in inflammation and autoimmunity

Cava, Antonio La

doi:10.1016/j.cyto.2016.10.011

Cited by 284 publications

(226 citation statements)

References 140 publications

Supporting

Mentioning

215

Contrasting

Unclassified

Order By: Relevance

“…Furthermore, the lactation number of the dams and serum leptin concentrations in their 1-week old calves were positively correlated (p = 0.0015; r = 0.4177). Leptin plays an important role in the onset of puberty and regulation of the immune system [40,41].…”

Section: Influence Of Mother's Parity On Early-and Late-weaned Calvesmentioning

confidence: 99%

Weaning Holstein Calves at 17 Weeks of Age Enables Smooth Transition from Liquid to Solid Feed

Schwarzkopf

Kinoshita

Kluess

et al. 2019

Animals

View full text Add to dashboard Cite

Simple Summary: Weaning calves from liquid to solid feed can be a stressful event in their life and can affect growth, development and welfare. It is commonly done at the age of 7 to 8 weeks on dairy farms, but weaning at a greater age could potentially reduce the associated stress. Therefore, it might improve growth rates and enable a smooth transition to an adult liver metabolism. To confirm this hypothesis this study evaluated the effect of two different weaning ages (7 vs. 17 weeks of age) on female Holstein calves. Furthermore, the effect of mothers' parity was analyzed (primiparous vs. multiparouos). Primiparous cows were often immature and still developing during their first pregnancy. This can lead to negative intrauterine conditions and result in long-term changes in the calf's metabolism. Late-weaned calves consumed high amounts of concentrate feed before weaning despite their high milk replacer intake, indicating the maturation of their rumen. In addition, they experienced a smooth transition to an adult liver metabolism as reflected by steady plasma glucose and cholesterol concentrations. Later weaning corrected the reduced growth of calves born to primiparous cows as well, indicating that those particularly benefitted from late weaning. All benefits were indicated by slower changes of blood metabolites and higher growth rates, which might lead to better health and productivity in their subsequent lifetime.Abstract: Development of calves depends on prenatal and postnatal conditions. Primiparous cows were still maturing during pregnancy, which can lead to negative intrauterine conditions and affect the calf's metabolism. It is hypothesized that weaning calves at higher maturity has positive effects due to reduced metabolic stress. We aimed to evaluate effects of mothers' parity and calves' weaning age on growth performance and blood metabolites. Fifty-nine female Holstein calves (38.8 ± 5.3 kg birth weight, about 8 days old) were used in a 2 × 2 factorial experiment with factors weaning age (7 vs. 17 weeks) and parity of mother (primiparous vs. multiparous cows). Calves were randomly assigned one of these four groups. Live weight, live weight gain and morphometry increased over time and were greater in calves weaned later. Metabolic indicators except total protein were interactively affected by time and weaning age. Leptin remained low in early-weaned calves born to primiparous cows, while it increased in the other groups. The results suggest that weaning more mature calves has a positive effect on body growth, and calves born to primiparous cows particularly benefit from this weaning regimen. It also enables a smooth transition from liquid to solid feed, which might reduce the associated stress of weaning.

show abstract

Section: Influence Of Mother's Parity On Early-and Late-weaned Calvesmentioning

confidence: 99%

Weaning Holstein Calves at 17 Weeks of Age Enables Smooth Transition from Liquid to Solid Feed

Schwarzkopf

Kinoshita

Kluess

et al. 2019

Animals

View full text Add to dashboard Cite

show abstract

“…These mice lack leptin due to a spontaneous homozygous mutation on the leptin gene, causing marked obesity, hyperinsulinemia, and hyperglycemia by 12 weeks of age. By approximately 24 weeks of age, ob/ob mice develop left ventricular hypertrophy and cardiac fibrosis and are in a proinflammatory state (La Cava, 2017). The C57BL/KsJ-db/db (db/db) mouse is a related genetic mouse model, which has a defective leptin receptor .…”

Section: Genetic Mouse Modelsmentioning

confidence: 99%

“…Importantly, endothelium-dependent aortic relaxation to acetylcholine (ACh) is impaired whereas that to direct nitric oxide donors remains unaffected, indicating endothelial dysfunction (Dong et al, 2010). Additionally, db/db mice have elevated circulating leptin which promotes a proinflammatory state, linked to the increased activity of interleukin-6 (IL-6) (La Cava, 2017). Neither ob/ob nor db/db mice, however, display increased blood pressure-unlike a large proportion of humans with metabolic syndrome-and are therefore not ideal models for the many such people with metabolic syndrome (Mark et al, 1999).…”

Section: Genetic Mouse Modelsmentioning

confidence: 99%

The Vascular Consequences of Metabolic Syndrome: Rodent Models, Endothelial Dysfunction, and Current Therapies

et al. 2020

View full text Add to dashboard Cite

Metabolic syndrome is characterized by visceral obesity, dyslipidemia, hyperglycemia and hypertension, and affects over one billion people. Independently, the components of metabolic syndrome each have the potential to affect the endothelium to cause vascular dysfunction and disrupt vascular homeostasis. Rodent models of metabolic syndrome have significantly advanced our understanding of this multifactorial condition. In this minireview we compare the currently available rodent models of metabolic syndrome and consider their limitations. We also discuss the numerous mechanisms by which metabolic abnormalities cause endothelial dysfunction and highlight some common pathophysiologies including reduced nitric oxide production, increased reactive oxygen species and increased production of vasoconstrictors. Additionally, we explore some of the current therapeutics for the comorbidities of metabolic syndrome and consider how these benefit the vasculature.

show abstract

“…Third, the BBSome regulates trafficking of the leptin receptor [28]. Leptin is a signaling molecule which acts as a pro-inflammatory cytokine [29,30]. In particular, leptin signaling inhibits the proliferation of regulatory T cells [31] and promotes the effector cell proliferation and polarization towards Th1 helper T cells [32].…”

Section: Introductionmentioning

confidence: 99%

Altered hematopoietic system and self-tolerance in Bardet-Biedl Syndrome

Tsyklauri

Niederlová

Forsythe

et al. 2020

Preprint

View full text Add to dashboard Cite

Bardet-Biedl Syndrome (BBS) is a pleiotropic genetic disease caused by dysfunction of primary cilia. The immune system of patients with BBS or another ciliopathy has not been investigated, most likely because hematopoietic cells do not form cilia. However, there are multiple indications that the impairment of the processes typically associated with cilia might influence the hematopoietic compartment and immunity. In this study, we analyzed clinical data of BBS patients as well as a corresponding mouse model of BBS4 deficiency. We uncovered that BBS patients have higher incidence of certain autoimmune diseases. BBS patients and animal models have elevated white blood cell levels and altered red blood cell and platelet compartments. Moreover, we observed that BBS4 deficiency alters the development and homeostasis of B cells in mice. Some of the hematopoietic system alterations were caused by the BBS-induced obesity.Overall, our study reveals a connection between a ciliopathy and the alterations of the immune system and the hematopoietic compartment.

show abstract

Leptin in inflammation and autoimmunity

Cited by 284 publications

References 140 publications

Weaning Holstein Calves at 17 Weeks of Age Enables Smooth Transition from Liquid to Solid Feed

Weaning Holstein Calves at 17 Weeks of Age Enables Smooth Transition from Liquid to Solid Feed

The Vascular Consequences of Metabolic Syndrome: Rodent Models, Endothelial Dysfunction, and Current Therapies

Altered hematopoietic system and self-tolerance in Bardet-Biedl Syndrome

Contact Info

Product

Resources

About