Periodontitis is a multifactorial chronic inflammatory disease associated with dysbiotic plaque biofilms and characterized by progressive destruction of the tooth-supporting apparatus. Globally, it is estimated that 740 million people are affected by its severe form. Periodontitis has been suggested to be linked to obesity and metabolic syndrome. Obesity, defined as excessive fat accumulation, is a complex multifactorial chronic inflammatory disease, with a high and increasing prevalence. Metabolic syndrome is defined as a cluster of obesity, dyslipidemia, hypertension, and dysglycemia. Obesity, metabolic syndrome and periodontitis are among the most common non-communicable diseases and a large body of evidence from epidemiologic studies supports the association between these conditions. Extensive research has established plausible mechanisms to explain how these conditions can negatively impact each other, pointing to a bidirectional adverse relationship. At present there is only limited evidence available from a few intervention studies. Nevertheless, the global burden of periodontitis combined with the obesity epidemic has important clinical and public health implications for the dental team. In accordance with the common risk factor approach for tackling non-communicable diseases, it has been proposed that oral healthcare professionals have an important role in the promotion of periodontal health and general well-being through facilitation of healthy lifestyle behaviours.

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The association of periodontal diseases with metabolic syndrome and obesity

Adipokines play a significant role in the pathogenesis of a low-grade inflammation associated with obesity and metabolic syndrome, and in chronic inflammatory and autoimmune diseases such as rheumatoid arthritis. Among variety of adipokines, resistin and visfatin are proposed as important pro-inflammatory mediators, which also interfere with the central regulation of insulin sensitivity. Resistin has been initially postulated as a risk factor for insulin resistance, however, the subsequent available data on it have revealed contradictory findings in both humans and rodents. On the other hand, visfatin has been suggested to be a beneficial adipokine with insulin-mimicking/-sensitizing effects, but regulation of visfatin production and its physiological importance in the conditions of obesity and type 2 diabetes mellitus are still not completely understood. Despite the opposing effects of resistin and visfatin on the regulation of insulin sensitivity, both adipokines have pro-inflammatory properties. Clinical and experimental studies have shown that the expression and secretion of resistin and visfatin are up-regulated during inflammation and in response to pro-inflammatory cytokines. It has also become increasingly evident that resistin as well as visfatin itself can contribute to the inflammatory processes by triggering cytokine production and NF-kappaB activation. New insight into the role of adipokines makes them attractive targets for novel therapeutic strategies in chronic inflammatory diseases or subclinical inflammation relating to obesity and various metabolic abnormalities.

/pdf/resistin-and-visfatin-regulators-of-insulin-sensitivity-4w5dkek71o.pdf

Resistin and visfatin: regulators of insulin sensitivity, inflammation and immunity.

Obesity is characterized by excess accumulation of lipids in adipose tissue and other organs, and chronic inflammation associated with insulin resistance and an increased risk of type 2 diabetes. Obesity, type 2 diabetes, and cardiovascular diseases are major health concerns. Resistin was first discovered as an adipose-secreted hormone (adipokine) linked to obesity and insulin resistance in rodents. Adipocyte-derived resistin is increased in obese rodents and strongly related to insulin resistance. However, in contrast to rodents, resistin is expressed and secreted from macrophages in humans and is increased in inflammatory conditions. Some studies have also suggested an association between increased resistin levels and insulin resistance, diabetes and cardiovascular disease. Genetic studies have provided additional evidence for a role of resistin in insulin resistance and inflammation. Resistin appears to mediate the pathogenesis of atherosclerosis by promoting endothelial dysfunction, vascular smooth muscle cell proliferation, arterial inflammation, and formation of foam cells. Indeed, resistin is predictive of atherosclerosis and poor clinical outcomes in patients with coronary artery disease and ischemic stroke. There is also growing evidence that elevated resistin is associated with the development of heart failure. This review will focus on the biology of resistin in rodents and humans, and evidence linking resistin with type 2 diabetes, atherosclerosis, and cardiovascular disease.

/pdf/resistin-in-rodents-and-humans-uxn9p9pkc8.pdf

Resistin in Rodents and Humans

The discovery of insulin 100 years ago and its application to the treatment of human disease in the years since have marked a major turning point in the history of medicine. The availability of purified insulin allowed for the establishment of its physiological role in the regulation of blood glucose and ketones, the determination of its amino acid sequence, and the solving of its structure. Over the last 50 years, the function of insulin has been applied into the discovery of the insulin receptor and its signaling cascade to reveal the role of impaired insulin signaling-or resistance-in the progression of type 2 diabetes. It has also become clear that insulin signaling can impact not only classical insulin-sensitive tissues, but all tissues of the body, and that in many of these tissues the insulin signaling cascade regulates unexpected physiological functions. Despite these remarkable advances, much remains to be learned about both insulin signaling and how to use this molecular knowledge to advance the treatment of type 2 diabetes and other insulin-resistant states.

Insulin action at a molecular level - 100 years of progress.

Physiological, pathological and potential therapeutic roles of adipokines.

Aim: The aim of the present study was to observe the effects of resistin on insulin sensitivity and glucose output in rat-derived hepatocytes. Methods: The rat hepatoma cell line H4IIE was cultured and stimulated with resistin; supernant glucose and glycogen content were detected. The insulin receptor substrate (IRS)-1 and IRS-2, protein kinase B/Akt, glycogen synthase kinase-3b (GSK-3b), the suppressor of cytokine signaling 3 (SOCS-3) protein content, as well as the phosphorylation status were assessed by Western blotting. Specific antisense oligodeoxynucleotides directed against SOCS-3 were used to knockdown SOCS-3.
 Results: Resistin induced insulin resistance, but did not affect glucose output in rat hepatoma cell line H4IIE. Resistin attenuated multiple effects of insulin, including insulin-stimulated glycogen synthesis and phosphorylation of IRS, protein kinase B/Akt, as well as GSK-3b. Resistin treatment markedly induced the gene and protein expression of SOCS-3, a known inhibitor of insulin signaling. Furthermore, a specific antisense oligodeoxynucleotide directed against SOCS-3 treatment prevented resistin from antagonizing insulin action. Conclusion: The major function of resistin on liver is to induce insulin resistance. SOCS-3 induction may contribute to the resistin-mediated inhibition of insulin signaling in H4IIE hepatocytes.

/pdf/resistin-induces-insulin-resistance-but-does-not-affect-126n7j563e.pdf

Resistin induces insulin resistance, but does not affect glucose output in rat-derived hepatocytes

AIM: To confirm whether insulin regulates resistin expression and secretion during differentiation of 3T3-L1 preadipocytes and the relationship of resistin with insulin resistance both in vivo and in vitro.

METHODS: Supernatant resistin was measured during differentiation of 3T3-L1 preadipocytes. L6 rat myoblasts and hepatoma cell line H4IIE were used to confirm the cellular function of resistin. Diet-induced obese rats were used as an insulin resistance model to study the relationship of resistin with insulin resistance.

RESULTS: Resistin expression and secretion were enhanced during differentiation 3T3-L1 preadipocytes. This cellular differentiation stimulated resistin expression and secretion, but was suppressed by insulin. Resistin also induced insulin resistance in H4IIE hepatocytes and L6 myoblasts. In diet-induced obese rats, serum resistin levels were negatively correlated with insulin sensitivity, but not with serum insulin.

CONCLUSION: Insulin can inhibit resistin expression and secretion in vitro, but insulin is not a major regulator of resistin in vivo. Fat tissue mass affects insulin sensitivity by altering the expression and secretion of resistin.

A paradox: insulin inhibits expression and secretion of resistin which induces insulin resistance.

Aim: To investigate the direct effects of resistin and resistin-binding peptide (RBP) on lipid metabolism and endocrine function in adipose tissue. Methods: Rat white adipose tissue was cultured in vitro and incubated for 24 h with 30 ng/mL recombinant rat resistin protein (rResistin) or combined with RBP of varying concentrations (1×10 -12 mol/L, 1×10 -10 mol/L, 1×10 -8 mol/L). Free fatty acids (FFA) released into medium was measured by a colorimetric kit. The levels of protein secretion and mRNA expression of TNF-α and adiponectin were detected by ELISA kit and RT-PCR respectively.
 Results: The levels of FFA released into medium were significantly increased after 24 h of exposure to rResistin, but significantly decreased after RBP was applied, although there was no difference between the 3 concentrations. The protein level and gene expression of TNF-α in adipose tissue were significantly increased after 24 h of exposure to rResistin, but only obviously decreased after incubated with 1×10 -8 mol/L RBP. The levels of protein secretion
and mRNA expression of adiponectin in adipose tissue were significantly decreased after 24 h of exposure to rResistin, but increased after incubated with RBP with the higher concentrations. Conclusion: RBP can effectively antagonize the role of resistin on the lipid metabolism and endocrine function of adipose tissue.

Resistin-binding peptide antagonizes role of resistin on white adipose tissue.

OBJECTIVE To investigate the effect of resistin overexpression on 3T3-L1 adipocyte lipid and glucose metabolism. METHODS Expression vector for rat resistin gene was constructed and transfected into 3T3-L1 adipocytes. Cell differentiation and lipid accumulation was determined by Oil Red O staining. Differentiation marker genes (pref-1, C/EBPalpha, FAS) and glucose transporter 4 (GLUT4) gene mRNA expressions were evaluated by reverse transcription-PCR (RT-PCR). Triglyceride (TG) and free fatty acids (FFAs) in adipocytes were measured by colorimetric kit. RESULTS (1) In resistin-overexpressed adipocytes, the lipid droplets presented at the second day which was earlier than the control cells. (2) The expression of C/EBPalpha and FAS genes in resistin-overexpressed adipocytes were up-regulated and the pref-1 was down-regulated compared with that of the control cells. (3) In resistin-overexpressed adipocytes, cellular TG and FFAs levels were significantly increased (P 0.05). CONCLUSION Overexpression of resistin can affect 3T3-L1 adipocyte lipid metabolism and thereby result in obesity and insulin resistance, but have no effect on GLUT4 gene expression.

Overexpression of resistin affect 3T3-L1 adipocyte lipid metabolism

OBJECTIVES
To investigate the changes in the rate and volume of mother's own milk (MOM) feeding for very low birth weight infants (VLBWIs) hospitalized during the prevention and control of the coronavirus disease 2019 (COVID-19) pandemic.


METHODS
A retrospective analysis was performed on the medical data of the VLBWIs with a gestational age of <32 weeks who were born and admitted to the Neonatal Intensive Care Unit of Nanjing Maternal and Child Health Hospital from January 2019 to December 2020. The changes in the rate and volume of MOM feeding for VLBWIs during hospitalization were examined.


RESULTS
A total of 301 VLBWIs were enrolled. According to the timing of COVID-19 outbreak, these infants were divided into a pre-CIVID-19 group with 205 VLBWIs and a post-COVID-19 group with 96 VLBWIs. Compared with the pre-CIVID-19 group, the post-COVID-19 group had a significantly lower rate of MOM feeding within 28 days after birth and during hospitalization (P<0.05), a significantly lower volume of MOM feeding within 0-7 days, 0-14 days, and 0-28 days after birth (P<0.05), and significantly higher incidence rates of moderate-to-severe bronchopulmonary dysplasia and feeding intolerance (P<0.05).


CONCLUSIONS
The COVID-19 pandemic has a significant impact on MOM feeding for VLBWIs, and there are significant reductions in the rate and volume of MOM feeding for VLBWIs within 28 days after birth, as well as a significant reduction in the rate of MOM feeding during hospitalization.

[Influence of the coronavirus disease 2019 pandemic on maternal breastfeeding for very low birth weight infants].

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