Many nutritional insults to the mother during the gestational or lactational period can affect the developing fetus and cause the onset of chronic diseases later in life, known as the "developmental origins of health and disease" (DoHad) hypothesis [1], [2], [3]. The perinatal period emerges as a critical window for brain maturation, neuronal differentiation, and adipogenesis, susceptible to epigenetic regulation [4]. This sensitivity extends to the hypothalamic circuitry governing energy balance and to adipocyte precursors, which are influenced by maternal metabolic conditions and nutritional factors [5]. However, the intricate interplay between melatonin (Mel), developmental programming, and the long-term health outcomes outlined in the DOHaD concept is not fully understood.

White adipose tissue (WAT) is related to energy metabolism through various processes, including lipolysis, lipogenesis, and energy storage in triacylglycerol [6]. Conversely, brown adipose tissue (BAT) is related to thermogenesis and cold homeostasis (heat production) [7]. Under specific conditions, white adipocytes can undergo adaptations, increasing the number of mitochondria and assuming a beige phenotype to produce thermogenesis and heat, a process called white adipocyte "browning" [8].

The hypothalamus controls thermogenesis in brown and beige adipose tissues. It integrates hormonal and neuronal signals in the sympathetic nervous system, mediates the adipose tissue-hypothalamus axis [9,10], and then influences the orexigenic and anorexigenic pathways [9].

The pineal gland secretes Mel (N-acetyl-5-methoxytryptamine) derived from the amino acid tryptophan in animals [10], and maternal Mel crosses the placenta, transmitting light and dark signals to the developing fetus [11]. In addition, various fetal tissues show Mel receptors responding to its anti-inflammatory properties [12], thus indicating a Mel role in fetal growth and development, epigenetically regulating fetal development [13].

We aimed to associate Mel's anti-inflammatory and antioxidant perspective with maternal obesity. Therefore, we studied long-term health outcomes outlined in the DOHaD concept by analyzing adult offspring's adipose tissue (WAT and BAT) and hypothalamus. We hypothesized that obese mother Mel supplementation could alleviate the detrimental effects of fetal programming linked to obesity.