Camel milk ameliorates steatohepatitis, insulin resistance and lipid peroxidation in experimental non-alcoholic fatty liver disease

Abstract

Background: Camel milk (CM) is gaining increasing recognition due to its beneficial effects in the control and prevention of multiple health problems. The current study aimed to investigate the effects of CM on the hepatic biochemical and cellular alterations induced by a high-fat, cholesterol-rich diet (HCD), specifically, non-alcoholic fatty liver disease (NAFLD).

Methods: Seventy male Wistar rats were divided into four groups: the Control (C) Group fed a standard diet; the Control + camel milk (CCM) Group fed a standard diet and CM, the Cholesterol (Ch) Group fed a HCD with no CM, and the Cholesterol + camel milk (ChM) Group fed a HCD and CM. The following parameters were investigated in the studied groups; basal, weekly random and final fasting blood glucose levels, intraperitoneal glucose tolerance test (GTT) and insulin tolerance test (ITT), serum insulin, serum lipids, liver functions, lipid peroxidation products, the antioxidant activity of catalase (CAT) and the levels of reduced glutathione (GSH). In addition, HOMA-IR as an index of insulin resistance (IR) and the histopathology of the hepatic tissue were assessed.

Results: The Ch Group developed features similar to those of non-alcoholic steatohepatitis (NASH), characterized by hepatic steatosis; inflammatory cellular infiltration in liver tissue; altered liver functions; and increased total cholesterol, triglycerides, low-density lipoprotein cholesterol, very-low-density lipoprotein cholesterol, atherogenic index (AI), blood glucose, IR, and malondialdehyde (MDA) levels. Additionally, feeding the HCD to animals in the Ch Group decreased CAT activity and the GSH and high-density lipoprotein (HDL) cholesterol levels. Camel milk intake for eight weeks decreased hepatic fat accumulation and inflammatory cellular infiltration, preserved liver function, increased the GSH levels and CAT activity, decreased the MDA levels, and ameliorated the changes in the lipid profile, AI, and IR in animals from the ChM Group.

Conclusions: CM has a unique composition that is rich in minerals; vitamins, insulin and insulin-like protein, and it increased HDL-cholesterol and ameliorated the biochemical and cellular features of NAFLD in rats that received a HCD. The antioxidant effect of CM is a likely mechanism for the altered metabolism and absorption of HCD in the presence of CM. Regular consumption of CM could provide a natural way to protect against NAFLD induced by a high-fat diet.

Figure 1

The changes in body weight (A), liver weight and liver to body weight ratio (B) in the control and the high-fat diet groups and the effect of camel milk intake at the end of the study. CCM; control + milk group, Ch; cholesterol group, ChM; cholesterol + milk group. Values are presented as the mean ± SD. † p < 0.05 versus control, ‡ p < 0.05 versus CCM, § p < 0.05 versus Ch, ¶ p < 0.05 versus ChM.

Figure 2

The changes in random blood glucose level (A), fasting blood glucose, serum insulin and HOMA-IR (B) in the control and high-fat diet treated groups and the effect of camel’s milk intake. CCM; control + milk group, Ch; cholesterol group, ChM; cholesterol + milk group. Values are presented as the mean ± SD. † p < 0.05 versus Control, ‡ p < 0.05 versus Control + camel milk, § p < 0.05 versus Cholesterol, ¶ p < 0.05 versus Cholesterol + camel milk.

Figure 3

Intraperitoneal glucose tolerance test (i.p GTT) (A), and insulin tolerance test (ITT) (B) in rats fed standard and high-fat diets with and without camel milk treatment for 8 weeks. CCM; control + milk group, Ch; cholesterol group, ChM; cholesterol + milk group. Values are presented as the mean ± SD.

Figure 4

Lipid profile and atherogenic index in rats fed standard and high-fat diets with and without camel milk treatment for 8 weeks. CCM; control+ milk group, Ch; cholesterol group, ChM; cholesterol+ milk group. Values are presented as the mean ± SD. † p < 0.05 versus control, ‡ p < 0.05 versus CCM, § p < 0.05 versus Ch, ¶ p < 0.05 versus ChM.

Figure 5

Gross and microscopic changes in the liver of the control and high-fat diet groups with and without camel milk intake. Part I: Gross macroscopic evaluation of the liver from the Control group (part A) and the control + camel milk Group (part B) showed red, smooth and shiny liver tissues. Livers from the Cholesterol Group (part C) that received the high-fat diet for eight weeks were extremely pale, enlarged, and extensively infiltrated with white spots that reflect fat accumulation inside the hepatic cells. The Cholesterol + milk group (part D) received camel milk for eight weeks, and the livers showed marked improvement compared to the livers of the untreated group; the livers were slightly pale with few scattered white spots compared with the Ch Group. Part II: 40X photomicrograph of the H and E stained liver tissue of the Control (part E) and the Control + milk groups (part F) showing normal polyhedral hepatocytes with a central nucleus and eosinophilic cytoplasm. In contrast, the Ch Group (part G) showed ballooning degeneration of the hepatocytes, loss of cytoplasmic eosin and eccentric nuclei, with diffuse microvesicular and macrovesicular steatosis, and foci of lobular inflammation and necrosis. Camel milk treatment in the ChM Group (part H) markedly attenuated the histopathological characteristics of NASH observed in the Ch Group. The ChM group showed only mild microvesicular steatosis, no inflammatory foci, and intact architecture.