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01 · ABSTRACT

Abstract

Background. Obesity involves the excessive expansion of white adipose tissue, typically associated with adipocyte hypertrophy and inflammation, especially in visceral depots, a process influenced by sex. Natural compounds like Copaiba’s oil (CO) exhibit anti-inflammatory and anti-adiposity effects, though their impact on white adipose tissue histology is unknown.

Aims. This study evaluated the effect of oral CO supplementation on the histology and content of visceral WAT depots in hypothalamic obese male and female Wistar rats.

Methods. The litter size was adjusted to 6-8 pups per dam (3-4 males and females) at birth. Hypothalamic obesity was induced in the neonatal period via subcutaneous injection of Monosodium L-glutamate (4g.Kg-1). Non-obese group received equimolar saline (1.25 kg-1). Half of the animals from each group received oral CO-supplementation (0.5mL.kg-1; three times/week) from pos natal days 30 to 90, while non-supplemented groups received saline (0.9%) during the same period, via and frequency. At 92 pos natal days, following 12h of fasting, the animals were euthanized, blood samples were collected, and plasma was used to dosage glucose and triglycerides from which the TyG index was calculated to evaluate insulin resistance. Visceral Perigonadal and Perirenal depots were excised, weighed, and analyzed histologically.

Results. CO-supplementation showed nonsignificant effects in non-obese groups (males or females). Obese male and female animals show higher triglycerides, increased insulin resistance, heavier visceral adipose tissue depots, lower adipocyte numbers, and increased hypertrophy than males and females non-obese. Moreover, obese males displayed hyperglycemia compared to non-obese males. CO supplementation's effects were sex-dependent in obese males, CO worsened triglyceride levels without affecting visceral adipose tissue content or histology. Conversely, in obese females, CO supplementation improved triglyceride levels, decreased perigonadal weight, and increased adipocyte numbers in perigonadal and perirenal depots.

Conclusion. Chronic oral CO supplementation does not prevent adipose tissue expansion or metabolic dysfunction in male hypothalamic obese rats. In contrast, obese female CO-supplemented showed a slight reduction in adiposity with increased adipocyte proliferation and improved fasting triglycerides levels, indicating greater responsiveness in females to the beneficial effects of CO on obesity.

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02 · PUBLICATION RECORD

Article details

JournalMedical Research Archives
IssueVol 12 No 10 (2024): October Issue, Issue 10, VOl.12
SectionResearch Articles
Published29 October 2024
DOI10.18103/mra.v12i10.5770
ISSN2375-1924
03 · RIGHTS & REUSE

Rights & reuse

This article is published under a Creative Commons Attribution License (CC BY 3.0) and may be shared or distributed by anyone as long as attribution is given to the journal.

Authors & affiliations

HK

Helen de França Kailer

Laboratory of Endocrine Physiology and Metabolism – LAFEM. Postgraduate Program in Biosciences and Health. State University of Western Paraná - UNIOESTE. Campus Cascavel – Paraná, Brazil.

ES

Elizangela Stein

Laboratory of Endocrine Physiology and Metabolism – LAFEM. Postgraduate Program in Biosciences and Health. State University of Western Paraná - UNIOESTE. Campus Cascavel – Paraná, Brazil.

MF

Marina Helena Forlin

Laboratory of Endocrine Physiology and Metabolism – LAFEM. Postgraduate Program in Biosciences and Health. State University of Western Paraná - UNIOESTE. Campus Cascavel – Paraná, Brazil.

EC

Eduarda Felchak Caldas

Laboratory of Endocrine Physiology and Metabolism – LAFEM. Postgraduate Program in Biosciences and Health. State University of Western Paraná - UNIOESTE. Campus Cascavel – Paraná, Brazil.

EG

Ellen Carolina Zawoski Gomes

Laboratory of Endocrine Physiology and Metabolism – LAFEM. Postgraduate Program in Biosciences and Health. State University of Western Paraná - UNIOESTE. Campus Cascavel – Paraná, Brazil.; Centro Universitário Fundação Assis Gurgacz – FAG. Cascavel. Paraná. Brazil.

ZG

Zoe Maria Neves de Carvalho Guareschi

Laboratory of Endocrine Physiology and Metabolism – LAFEM. Postgraduate Program in Biosciences and Health. State University of Western Paraná - UNIOESTE. Campus Cascavel – Paraná, Brazil.

MU

Marianela Andrea Díaz Urrutia

Laboratory of Endocrine Physiology and Metabolism – LAFEM. Postgraduate Program in Biosciences and Health. State University of Western Paraná - UNIOESTE. Campus Cascavel – Paraná, Brazil.

SD

Sirlei Patrícia de Souza

Laboratory of Endocrine Physiology and Metabolism – LAFEM. Postgraduate Program in Biosciences and Health. State University of Western Paraná - UNIOESTE. Campus Cascavel – Paraná, Brazil.

BD

Beatriz Daudt

Laboratory of Endocrine Physiology and Metabolism – LAFEM. Postgraduate Program in Biosciences and Health. State University of Western Paraná - UNIOESTE. Campus Cascavel – Paraná, Brazil.

BS

Bruna Schumaker Siqueira

Laboratory of Endocrine Physiology and Metabolism – LAFEM. Postgraduate Program in Biosciences and Health. State University of Western Paraná - UNIOESTE. Campus Cascavel – Paraná, Brazil.

SG

Sabrina Grassiolli

Laboratory of Endocrine Physiology and Metabolism – LAFEM. Postgraduate Program in Biosciences and Health. State University of Western Paraná - UNIOESTE. Campus Cascavel – Paraná, Brazil.

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