Distinct utilization of biotin in and between adipose and brain during aging is associated with a lipogenic shift in Wistar rat brain.

Tissue-specific metabolism determines their functions that collectively sense and respond to numerous stress cues to achieve systemic homeostasis. Chronic stress skews such metabolic profiles and leads to failure of organs as evidenced by a bias towards lipid synthesis and storage in the aging brain, muscle, and liver under Alzheimer's disease, sarcopenia, and non-alcoholic fatty liver disease, respectively. In contrast, the tissue destined for lipid synthesis and storage, such as adipose, limits its threshold and develops diabetes mellitus.

Astroglial biotin deprivation under endoplasmic reticulum stress uncouples BCAA-mTORC1 role in lipid synthesis to prolong autophagy inhibition in the aging brain.

Autophagy delays the onset of endoplasmic reticulum (ER) stress by recycling cellular debris. However, the cues that elicit autophagy under the emergence of ER stress and their dysregulation during aging remains obscure. Amino acids, notably branched-chain amino acids (BCAA), get accumulated in the cells once protein synthesis is inhibited by ER stress.

Autophagy inhibition by biotin elicits endoplasmic reticulum stress to differentially regulate adipocyte lipid and protein synthesis.

Biotin is an indispensable adipogenic agent, and its ability to coordinate carbohydrate, lipid, and amino acid metabolism sensitizes insulin signaling in adipocytes. This enables the organism to adapt and survive under nutrient stress by synthesis and storage of lipids. Biotin deficiency mimics insulin resistance with alterations in cellular intermediary metabolism.

Thymoquinone inhibits cell proliferation through regulation of G1/S phase cell cycle transition in N-nitrosodiethylamine-induced experimental rat hepatocellular carcinoma.

Dysregulated cell proliferation and tumorigenesis is frequently encountered in several cancers including hepatocellular carcinogenesis (HCC). Thus, agents that inhibit cell proliferation and restrain hepatic tumorigenesis through cell cycle regulation have a beneficial effect in the treatment of hepatocellular carcinogenesis. The present study was aimed to investigate the efficacy of thymoquinone (TQ), an active compound derived from the medicinal plant Nigella sativa, on N-nitrosodiethylamine (NDEA) [0.

Polyherbal formulation Bresol® protects the mast cells against compound 48/80-induced disruption and histamine release: a non-immunological mechanism of mast cell stabilization.

Objective: Present study was aimed to evaluate the protective effect of Bresol®, a polyherbal formulation, on mast cell degranulation and histamine release from mast cells.

Methods: Mast cell-stabilizing activity of Bresol® was evaluated against compound 48/80-induced mast cell degranulation and histamine release from rat peritoneal mast cells in ex vivo conditions.

Results: Microscopy of the control group smears showed more of intact mast cells, with very minimum number of degranulated mast cells and negligible amount of histamine release.