Pandarinath Savitikadi

Obesity is a multifactorial metabolic disorder associated with insulin resistance, oxidative stress, and excessive accumulation of advanced glycation end-products (AGEs). Emerging evidence suggests that aldose reductase (AR), a key enzyme of the polyol pathway, also contributes to obesity-associated metabolic dysfunction. In this study, we evaluated the potential of a functional food mix (FFM) containing Emblica officinalis, Zingiber officinale, Curcuma longa, Piper nigrum, Cinnamomum zeylanicum, and Capsicum annuum in specific proportions to prevent obesity by targeting AR inhibition and AGE accumulation. Male WNIN/GR-Ob obese rats were randomised into untreated obese, low-dose FFM (FF1), and high-dose FFM (FF2) groups, while lean littermates served as controls. Animals received the respective experimental diets for 6 months. Body weight, food intake, body composition (DEXA), biochemical parameters, carboxymethyl lysine (CML; a major AGE), and hepatic AR activity were assessed. FFM supplementation significantly attenuated body weight gain by 9 and 22% and reduced total fat mass by 8 and 23% with FF1 and FF2, respectively, with greater efficacy at the higher dose. Both doses lowered circulating leptin (p < 0.05), while FF2 significantly improved insulin sensitivity by reducing plasma insulin and HOMA-IR (p < 0.05). FFM also markedly decreased plasma CML concentrations and hepatic AR activity. Furthermore, treatment increased adiponectin levels, improved hypertriglyceridemia and hypercholesterolemia, and reduced lipid peroxidation (p < 0.05). Together, these findings suggest that the novel functional food mix exerts potent anti-obesity effects through inhibition of AR, suppression of AGE accumulation, and attenuation of oxidative stress.

Aging-related muscle atrophy/sarcopenia is the most common type of muscle impairment that affects the quality of life. In the current study, we examined the effect of a functional food mixture of amla, turmeric, black pepper, cinnamon, and ginger on D-galactose-induced muscle alterations in rats. Wistar rats were randomly divided into three groups: Control (C), D-galactose (G), and D-galactose + functional food mixture intervention (G + I). Rats in group-G and -G + I were injected with D-galactose (300 mg/kg/day) for 90 days. After 3 months of the experimental period, the rats were sacrificed to collect gastrocnemius muscle. Group-G rats showed elevated levels of inflammatory cytokines (TNFα and NF-kB), atrogenes (atrogin-1 and MuRF1), decreased insulin/IGF1 signaling (decreased AKT phosphorylation), altered mitochondrial dynamics (increased fission and decreased fusion proteins), increased apoptotic mediators (Bax/Bcl-2, and caspase-3), and decreased muscle cell cross-sectional area when compared with group-C ( p < 0.05). Interestingly, supplementation with the functional food mixture prevented galactose-induced alterations in the muscle. The observed anti-inflammatory, insulin-sensitizing, mitochondria-protective, and antiapoptotic effects of the functional food could be the underlying mechanisms in displaying positive effects against galactose-induced muscle atrophy and, hence, may be useful for the prevention of age-related muscle disorders.

Several studies suggest that the maternal protein content and source can affect the offspring’s health. However, the chronic impact of maternal quality and quantity protein restriction, and reversible changes upon rehabilitation, if any, in the offspring, remains elusive. This study examined the effects of maternal low-quality protein (LQP) and low-protein (LP) intake from preconception to post-weaning, followed by rehabilitation from weaning, on body composition, glucose-homeostasis, and metabolic factors in rat offspring. Wistar rats were exposed to normal protein (NP; 20% casein), LQP (20% wheat gluten) or LP (8% casein) isocaloric diets for 7 weeks before pregnancy until lactation. After weaning, the offspring were exposed to five diets: NP, LQP, LQPR (LQP rehabilitated with NP), LP, and LPR (LP rehabilitated with NP) for 16 weeks. Body composition, glucose-homeostasis, lipids, and plasma hormones were investigated. The LQP and LP offspring had lower bodyweight, fat and lean mass, insulin and HOMA-IR than the NP. The LQP offspring had higher cholesterol, T3 and T4, and lower triacylglycerides and glucose, while these were unaltered in LP compared to NP. The majority of the above outcomes were reversed upon rehabilitation. These results suggest that the chronic exposure of rats to maternal LQP and LP diets induced differential adverse effects by influencing body composition and metabolism, which were reversed upon rehabilitation.