The beneficial effects of the composite probiotics from camel milk on glucose and lipid metabolism, liver and renal function and gut microbiota in db/db mice

Abstract

Background: Probiotics may have beneficial effects on patients with type 2 diabetes mellitus (T2DM). We separated 4 lactobacillus and 1 saccharomycetes from traditional fermented cheese whey (TFCW) and prepared composite probiotics from camel milk (CPCM) and investigated their effects on glucose and lipid metabolism, liver and renal function and gut microbiota in db/db mice.

Methods: CPCM was prepared in the laboratory and 40 db/db mice were randomly divided into 4 groups as metformin, low-dose and high-dose group and model group, and treated for 6 weeks. In addition, 10 C57BL/Ks mice as normal control group were used for comparison. Fasting blood glucose (FBG), body weight (BW), oral glucose tolerance test (OGTT), glycated hemoglobin (HbAlc), C-peptide (CP), triglycerides (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high density lipoprotein cholesterol (HDL-C), 24 h urinary microalbumin (24 h malb), urine ketone, urine sugar, pancreas and liver tissue and intestinal flora were tested.

Results: Compared to diabetic group, high dose CPCM significantly decreased FBG, OGTT, HbAlc and IRI, plasma TC, TG, LDL-C, 24 h malb, urine ketone and urine sugar, increased CP, HDL-C levels, improved the liver and kidney function, protected the function of islets, also increased intestinal tract lactic acid bacteria and Bifidobacterium, decreased Escherichia in db/db mice.

Conclusion: CPCM decreased FBG, OGTT and HbAlc, increased CP, modulated lipid metabolism and improved liver and kidney protected injury in db/db mice, which may be related to various probiotics acting through protecting the function of islets and regulating intestinal flora disturbance.

Keywords: Composite probiotics camel milk; Gut microbiota; TFCW; TG; db/db mice.

Fig. 1

Effects of CPCM on body weight and Fasting blood glucose in db/db mice. ^***P < 0.001 VS normal group; ^# P < 0.05, ^## P < 0.01 and ^### P < 0.001 VS model group. a. Body weight (g); b. Fasting blood glucose (mmol/L)

Fig. 2

Effect of CPCM on AUC, glycosylated hemoglobin, C-peptide and insulin resistance index in db/db mice. ^*P < 0.05, ^***P < 0.001 vs normal group; ^# P < 0.05, ^## P < 0.01, and ^### P < 0.001 vs model group. a. AUC; b. glycosylated hemoglobin (ng/ml); c. C-peptide (mmol/L); d. insulin resistance index

Fig. 3

Effects of CPCM on lipid metabolism, liver weight and liver index in db/db mice. ^*** P < 0.001 vs normal group; ^# P < 0.05 and ^### P < 0.001 vs model group. a. Triglyceride (mmol/L); b. Total cholesterol (mmol/L); c. High density lipoprotein-cholesterol (mmol/L); d. Low density lipoprotein-cholesterol (mmol/L); e. Liver wet weight (g); f. Liver index (10²)

Fig. 4

Effect of CPCM on renal weight and index and 24 h microalbuminuria in db/db mice. ^** P < 0.01, ^*** P < 0.001vs normal group; ^# P < 0.05 vs model group. a. Renal wet weight (g); b. Renal index (10³); c.24 h microalbuminuria (ug·24 h^− 1)

Fig. 5

The starting copy number of Escherichia and Bifidobacterium in db/db mice. ^** P < 0.01 vs normal group; ^# P < 0.05, ^## P < 0.01 vs model group. a. Escherichia; b. Bifidobacterium

Fig. 6

Histological analyses of the effects of CPCM on pancreas and liver in db/db mice. Hematoxylin-eosin (HE) stained pancreatic(a) microsections(original magnification 400×) and hepatic(b) microsections (original magnification 400×) (n = 4 images/group)