Metformin Ameliorates Treatment of Obese Type 2 Diabetic Patients with Mental Retardation; its Effects on Eating Behavior and Serum Leptin Levels

Abstract

The metabolic effects of a biguanide, metformin, on glycemic control and eating behavior were investigated in 16 type 2 diabetic subjects with mental retardation who were habitual overeaters and had difficulty in controlling their appetites. The subjects (n = 16) received metformin (750 mg/day) for 6 months and body weight, body mass index (BMI) were measured monthly. They had repetitive metabolic and hormonal studies. Their eating behavior was analyzed by questionnaires given by their guardians before and after treatment. Metformin treatment significantly reduced their body weights (p < 0.01), body mass index (BMI) (p < 0.01), the levels of HbA1c (p < 0.001), fasting blood glucose (FBG) (p < 0.05), serum insulin (p < 0.05), C-peptide (p < 0.01), triglyceride (p < 0.01), and total cholesterol (p < 0.05). Insulin resistance index (FBG (mg/dl) x serum insulin levels ( micro U/ml) x 1/405) was significantly reduced after 1-month treatment. The serum leptin levels were significantly decreased after 4 month's treatment and thereafter (p < 0.05). Analysis of the questionnaires before and after treatment showed that the daily intake of regular and additional foods significantly decreased after treatment (p < 0.01 and p < 0.001, respectively) with improvements of eating behavior. We conclude that metformin may have beneficial effects not only to control glycemia but also to correct eating behavior in obese type 2 diabetic patients with the difficulty in controlling their appetites. The improvement was related to the reduction of insulin resistance and serum leptin levels.

Are the beneficial cardiovascular effects of simvastatin and metformin also associated with a hormone-dependent mechanism improving insulin sensitivity?

“…Despite a metformin-induced weight loss and probably fat mass loss, this medication did not induce changes in leptin concentrations. Contrasting findings were observed in other studies which detected a reduction in leptin levels in obese type 2 diabetic patients (31). Our inability to demonstrate an effect of metformin therapy on leptin and adiponectin levels in metabolic disturbed subjects is in agreement with other studies (32)(33)(34).…”

Effects of metformin on weight loss

“…Metformin promotes weight loss by reducing food intake, as changes in total daily energy expenditure are not evident [5,9,14,15]. Interestingly, decreases in meal size are noticed during initial metformin treatment, whereas reductions in meal number continue over time [16 && ].…”

Nutrition and Adults With Intellectual or Developmental Disabilities: Systematic Literature Review Results*

“…However, published reports on biochemical testing of adults with intellectual or developmental disabilities are few and limited to dehydration and serum concentration of urea and electrolytes (Macdonald et al, 1989); CVD risk factors, such as blood lipids (Bertoli et al, 2006;Braunschweig et al, 2004;Draheim, McCubbin, & Williams, 2002;Draheim et al, 2002a;Rimmer et al, 1994), Creactive protein (Butler, Bittel, Kibiryeva, & Garg, 2006), and blood glucose and insulin (Bertoli et al, 2006;Braunschweig et al, 2004;Draheim, McCubbin, & Williams, 2002;Draheim et al, 2002a); bone health, including vitamin D status and markers of bone remodeling (Center, Beange, & McElduff, 1998;Wong, Lau, Lim, & Fung, 2006;Zubillaga et al, 2006); iron-and copper-related anemias (Molteno et al, 2000;Razagui et al, 1991); vitamins B 12 (Morad, Gringols, Kandel, & Merrick, 2005) and B 6 (Ellman et al, 1986); other nutrient deficiencies (Cole et al, 1985); and appetite and fat-deposition hormones, including leptin (Cento et al, 1999;Hoybye, Barkeling, Espelund, Petersson, & Thoren, 2003;Komori et al, 2004;Proto et al, 2007;Weigle et al, 1997), ghrelin (DelParigi et al, 2002Goldstone et al, 2004Goldstone et al, , 2005, and neuropeptide Y and oxytocin (Hoybye et al, 2003). Table 4 summarizes our review of reports on biochemical assessments of nutritional status and risk in adults with intellectual or developmental disabilities.…”