Evaluation of serum leptin and adiponectin in obese individuals with chronic periodontitis

Boyapati, Ramanarayana; Chintalapani, Srikanth; Ramisetti, Arpita; Salavadhi, Shyam Sunder; Ramachandran, Radhika

doi:10.4103/ccd.ccd_1_18

Cited by 17 publications

(17 citation statements)

References 13 publications

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“…Elevated plasma and gingival crevicular fluid levels of pro-inflammatory adipokines (leptin, resistin) and decreased levels of the anti-inflammatory adipokine adiponectin have been reported. [75][76][77] These studies demonstrate that the low-grade inflammatory state in obesity is associated with increased levels of proinflammatory mediators in the periodontium. Cytokines, such as interleukin-1beta and tumor necrosis factor-alpha, promote recruitment of immunoinflammatory cells, and production of proteases and bone resorption.…”

Section: Inflammationmentioning

confidence: 66%

The association of periodontal diseases with metabolic syndrome and obesity

Jepsen

Suvan

Deschner³

2020

Periodontology 2000

192

178

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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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Section: Inflammationmentioning

confidence: 66%

The association of periodontal diseases with metabolic syndrome and obesity

Jepsen

Suvan

Deschner³

2020

Periodontology 2000

192

178

View full text Add to dashboard Cite

show abstract

“…In obese subjects with periodontitis, pro-inflammatory cytokines (Interleukin-1β (Il-1β), Interleukin-6 (Il-6), Tumor Necrosis Factor α (TNF-α)) were found in greater quantities in the blood and also in the crevicular gingival fluid compared to normo-weighted subjects with periodontitis [ 35 , 36 ]. In the crevicular gingival fluid, the level of pro-inflammatory adipokines (leptin, visfatin, and resistin) is also increased in obese subjects [ 37 , 38 ]. The increase of pro-inflammatory cytokines and adipokines in periodontal tissues promotes bone resorption processes caused by the recruitment of immuno-inflammatory cells [ 39 , 40 ].…”

Section: Discussionmentioning

confidence: 99%

Obesity Drives an Oral Microbiota Signature of Female Patients with Periodontitis: A Pilot Study

et al. 2021

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The aim of this study was to analyze the link between oral microbiota and obesity in humans. We conducted a pilot study including 19 subjects with periodontitis divided into two groups: normo-weighted subjects (NWS) with a body mass index (BMI) between 20 and 25 (n = 9) and obese subjects (OS) with a BMI > 30 (n = 10). Obesity was associated with a poor oral health status characterized by an increased number of missing teeth and a higher score of periodontal-support loss associated with dysbiotic oral microbiota (39.45 ± 3.74 vs. 26.41 ± 11.21, p = 0.03 for the Chao 1 index). Oral microbiota taxonomic analysis showed that the abundance of the Capnocytophaga genus was higher (2.47% ± 3.02 vs. 0.27% ± 0.29, p = 0.04) in OS compared to NWS. Obese females (OF) were characterized by an increase in the Streptococcus genus (34.12% ± 14.29 vs. 10.55% ± 10.42, p = 0.05) compared to obese males (OM), where the Neisseria genus was increased (5.75% ± 5.03 vs. 58.05% ± 30.64, p = 0.008). These first data suggest that sex/gender is determinant in the link between oral dysbiotic microbiota and obesity in patients with periodontitis. Our results could lead to recommendations concerning therapeutic strategies for obese patients with periodontitis following the sex/gender.

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“… 23 – 26 High leptin levels occur in obesity. 40 , 41 In our previous study, we found that GnRH levels could be inhibited by high leptin levels. 16 From this study, higher leptin levels were also found in DIO mice with DEHP exposure.…”

Section: Discussionmentioning

confidence: 90%

Combined effects of obesity and di-(2-ethylhexyl) phthalate on testosterone levels and kisspeptin/GPR54 expression in hypothalamus and testes of male mice

Zhai

Zhao

Bai

et al. 2020

Journal of the Chinese Medical Association

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Background: This study evaluated whether obese male mice exposed to di-(2-ethylhexyl) phthalate (DEHP) showed synergistic effects on testosterone levels and the potential underlying mechanism. Methods: Forty-eight male mice were assigned to six groups for 12-week treatments as follows: normal, DEHP100, diet-induced obesity (DIO), DIO + DEHP30, DIO + DEHP100, and DIO + DEHP300. Serum hormone levels, including testosterone (T), luteinizing hormone (LH), and leptin, were detected by ELISA. The levels of Ob-R, kisspeptin, and GPR54 protein expression in hypothalamus and testicular tissues were measured by western blot. Results: There were significantly lower levels of serum T and LH, higher levels of serum leptin and Ob-R, and kisspeptin and GPR54 protein expression were reduced in hypothalamus and testicular tissues in the DIO and DEHP groups compared with controls. Moreover, serum T and leptin levels were more severe in the combined DIO and DEHP exposure group than in the single exposure groups. Serum LH levels and GPR54 expression in the testis were significantly decreased in DIO + DEHP300 mice compared with DIO mice ( p < 0.05). Conclusion: Obesity- and DEHP-only exposure had adverse effects on testosterone levels in mice, which may be due to high leptin levels and decreased Ob-R, kisspeptin, and GPR54 expression. Obesity combined with DEHP exposure had an additive adverse effect on testosterone levels in mice. One of the potential mechanisms is higher leptin levels and decreased GPR54 expression in the testes.

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Evaluation of serum leptin and adiponectin in obese individuals with chronic periodontitis

Cited by 17 publications

References 13 publications

The association of periodontal diseases with metabolic syndrome and obesity

The association of periodontal diseases with metabolic syndrome and obesity

Obesity Drives an Oral Microbiota Signature of Female Patients with Periodontitis: A Pilot Study

Combined effects of obesity and di-(2-ethylhexyl) phthalate on testosterone levels and kisspeptin/GPR54 expression in hypothalamus and testes of male mice

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