Abstract
Camel milk (CM) has a unique composition rich in antioxidants, trace elements, immunoglobulins, insulin, and insulin-like proteins. Treatment by CM demonstrated protective effects against nonalcoholic fatty liver disease (NAFLD) induced by a high-fat cholesterol-rich diet (HFD-C) in rats. CM dampened the steatosis, inflammation, and ballooning degeneration of the hepatocytes. It also counteracted hyperlipidemia, insulin resistance (IR), glucose intolerance, and oxidative stress. The commencement of NAFLD triggered the peroxisome proliferator-activated receptor-α (PPAR-α), carnitine palmitoyl-transferase-1 (CPT1A), and fatty acid-binding protein-1 (FABP1) and decreased the PPAR-γ expression in the tissues of the animals on HFD-C. This was associated with increased levels of the inflammatory cytokines IL-6 and TNF-α and leptin and declined levels of the anti-inflammatory adiponectin. Camel milk treatment to the NAFLD animals remarkably upregulated PPARs (α, γ) and the downstream enzyme CPT1A in the metabolically active tissues involved in cellular uptake and beta-oxidation of fatty acids. The enhanced lipid metabolism in the CM-treated animals was linked with decreased expression of FABP1 and suppression of IL-6, TNF-α, and leptin release with augmented adiponectin production. The protective effects of CM against the histological and biochemical features of NAFLD are at least in part related to the activation of the hepatic and extrahepatic PPARs (α, γ) with consequent activation of the downstream enzymes involved in fat metabolism. Camel milk treatment carries a promising therapeutic potential to NAFLD through stimulating PPARs actions on fat metabolism and glucose homeostasis. This can protect against hepatic steatosis, IR, and diabetes mellitus in high-risk obese patients.
Highlights
The global upsurge in the incidence of obesity, type II diabetes mellitus (DM), and the metabolic syndrome has boosted the incidence of nonalcoholic fatty liver disease (NAFLD) [1]
The animals were randomly divided into four experimental groups (n = 10 in each): control group: control healthy animals receiving no camel milk treatment; control+Camel milk (CM) group: control healthy animals receiving camel milk treatment; NAFLD group: animals with nonalcoholic fatty liver disease (NAFLD) receiving no treatment; and NAFLD+CM group: animals with NAFLD treated with camel milk
There was no significant change of the peroxisome proliferator-activated receptor-α (PPAR-α) proteins in the liver of the healthy control+CM group receiving CM in comparison to the non treated control group (p > 0:05)
Summary
The global upsurge in the incidence of obesity, type II diabetes mellitus (DM), and the metabolic syndrome has boosted the incidence of nonalcoholic fatty liver disease (NAFLD) [1]. Multiple risk factors have been linked with the incidence of NAFLD including: genetic predisposition, lack of physical activity, high caloric intake, oxidative stress, inflammatory cytokines, gut infections, and impaired immune response [3, 4]. The first stage of the pathophysiology of NAFLD involves increased fat deposition in the hepatocytes which is referred to as hepatic steatosis. This can progress to nonalcoholic steatohepatitis (NASH) characterized by more susceptibility to hepatocyte injury and death by inflammation, oxidative stress, gut bacterial endotoxins, and mitochondrial dysfunction [5]. Activation of the hepatic stellate cells increases extracellular matrix deposition leading to fibrosis
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