These results suggest that the chromium picolinate/biotin combination, administered as an adjuvant to current prescription anti-diabetic medication, can improve glycaemic control in overweight to obese individuals with type 2 diabetes; especially those patients with poor glycaemic control on oral therapy.

Dyslipidemia, often found in type 2 diabetes mellitus (T2DM) patients, plays an important role in the progression of cardiometabolic syndrome. Two essential nutrients, chromium and biotin, may maintain optimal glycemic control. The authors report here a randomized, double-blind placebo-controlled trial (N=348; chromium picolinate and biotin combination [CPB]: 226, placebo: 122; T2DM participants with hemoglobin A1c [HbA1c] >or=7%) evaluating the effects of CPB on lipid and lipoprotein levels. Participants were randomly assigned (2:1 ratio) to receive either CPB (600 microg chromium as chromium picolinate and 2 mg biotin) or a matching placebo once daily for 90 days. Statistical analyses were conducted in all eligible participants. Subsequent supplemental analyses were performed in T2DM participants with hypercholesterolemia (HC) and in those using stable doses of statins. In the primary analysis, CPB lowered HbA1c (P<.05) and glucose (P<.02) significantly compared with the placebo group. No significant changes were observed in other lipid levels. In participants with HC and T2DM, significant changes in total cholesterol and low-density lipoprotein cholesterol (LDL-C) levels and atherogenic index were observed in the CPB group (P<.05). Significant decreases in LDL-C, total cholesterol, HbA1c , and very low-density cholesterol levels (P<.05) were observed in the CPB group taking statins. CPB treatment was well tolerated with no adverse effects, dissimilar from those associated with placebo. These data suggest that intervention with CPB improves cardiometabolic risk factors.

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Since the carbohydrate reserves in amphibian eggs are mainly stored as glycogen (Gregg, 1948), attempts have been made to estimate its utilization during development as a function of glycogen breakdown. The most reliable data show that glycogen level begins to decrease when time of gastrulation starts (Brachet and Needham, 1935 ;Gregg. 1948). This has been confirmed by microchemical (Heatley and Lindahl, 1937;Jaeger, 1945) as well as histochemical methods (Woerdemann, 1933;Raven, 1935) which have also shown that glycogenolysis is stronger in those cells involved in the morphogenetic movements of gastrulation. Besides, the determination of the respiratory quotient (R.Q.) has given values concordant with those results. It is true that Earth (1946) has found a constant value of about 0.9; but Brachet (1934) and Boell (1955) have reported low values during segmentation, with a tendency to increase up to a value close to 1 at the time of gastrulation.Less is known about the egg enzymes involved in glycogenolysis. Some evidence was reported indicating that glycogen breakdown could be accomplished through phosphoroclastic (Cohen, 1954;Gregg et al, 1964) as well as through amylolytic pathways (see Urbani, 1962, for a review of the subject). The most outstanding news reported by the Italian author was the description of a ^-amylasic activity in eggs of Rana escnlcnta and Biijo vulgaris.Nothing is known, however, about glycogenolytic enzymes in Bufo arenarum.The limited information we possess on glycogen utilization during development agrees with the above reported results. Thus, a glycogen loss in eggs could be detected after the onset of gastrulation (Barbieri and Gil, 1962) ; and the R.Q. values were found to increase from about 0.6 during segmentation, up to 1 at the time of gastrulation (Legname and Barbieri, 1962).

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